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PubMed2005

Role of quantitative CT in predicting hypoxemia and complications after lung lobectomy for cancer, with special reference to area of emphysema.

STUDY OBJECTIVES: To determine the ability of quantitative CT, with special reference to area of emphysema, to predict early postoperative oxygenation capacity and outcome after lung lobectomy for cancer. METHODS: Sixty-two consecutive patients scheduled to undergo lung lobectomy for cancer were enrolled in this study. The area of emphysema (< - 910 Hounsfield units) was measured on a three-dimensional CT lung model. Arterial oxygen saturation (Sao(2)) was calculated from Pao(2) measured 1 day before and 1 day after surgery with patients at rest breathing room air. A patient was considered to have recovered at the completion of a standardized management regimen. RESULTS: Postoperative Sao(2) (postSao(2)) was predicted by the baseline value and the area of emphysema with the use of a regression equation. Ten of the 62 patients (16%) had postoperative cardiopulmonary complications (CPCs). The median time to postoperative recovery was 3 days (range, 1 to 17 days). Predicted postSao(2) and predicted postoperative FEV(1) were shown to be significant independent predictors of postoperative CPCs as well as postoperative recovery time. CONCLUSION: Determining the area of emphysema by quantitative CT is useful in predicting early postoperative oxygenation capacity. Predicted oxygenation capacity and predicted ventilatory capacity independently affect perioperative outcomes. Therefore, using quantitative CT in combination with spirometry may improve risk prediction in patients undergoing lung lobectomy for cancer. However, the role of quantitative CT in grading nonemphysematous lung diseases, such as interstitial lung diseases, must be investigated.

Aged↗
PubMed1976

The spirographic "kink". A sign of emphysema.

The significance of the "kink" occurring in the early portion of the forced expiratory spirogram of some patients with obstructed airflow was investigated in 153 patients with chronic obstructive pulmonary disease or asthma. The kink, which is presumably due to airway collapse, is facilitated by the presence of emphysema, which results in loss of elastic recoil, a positive pleural pressure, high bronchiolar resistance, and structural weakness in the walls of the major airways. A significant reduction of carbon-monoxide diffusing capacity was used as the indicator of the presence of significant anatomic emphysema. Eighty percent (39) of 49 patients with the spirographic kink had a low diffusing capacity, whereas only 16 of those without the kink had significantly impaired diffusion. Seventy percent (39) of the 56 patients who had emphysema by this criterion demonstrated a spirographic kink. This test is, therefore, offered as a simple, effective, and widely applicable screening procedure for detecting emphysema, with a low incidence of false-positive results.

Asthma↗
PubMed1989

Pathogenesis of emphysema. Assessment of basic science concepts through clinical investigation.

It is clear that alpha 1AT deficiency leads to early onset pulmonary emphysema. With the lead provided by the deficiency state, studies aimed at the linkage between alpha 1AT and its target enzyme, neutrophil elastase, have provided useful information about the pathogenesis of emphysema due to cigarette smoking. alpha 1AT represents the predominant antielastase of the lower respiratory tract. This observation implicates neutrophil elastase as the enzyme responsible for lung destruction, since affinity studies demonstrate that alpha 1ATs physiologically relevant function is the inhibition of neutrophil elastase. However, because of the inexorably slow nature of the emphysema process, demonstration of the protease-antiprotease imbalance in the lungs of smokers has been difficult. Studies using sensitive assays for alpha 1AT function and for neutrophil elastase's presence have added new support for the protease-antiprotease theory, and evaluation of related disorders such as the adult respiratory distress syndrome and cystic fibrosis have provided corraborative evidence. Finally, studies that have indicated that the major site of the protease-antiprotease imbalance is the microenvironment of protease-producing cells offer a new direction for future research into the pathogenesis of emphysema.

Bronchoalveolar Lavage Fluid↗
PubMed2005

Emphysema in alpha1-antitrypsin deficiency: does replacement therapy affect outcome?

Severe alpha(1)-antitrypsin (AAT) deficiency is an inherited disorder that leads to the development of emphysema in smokers at a relatively young age; most are disabled in their forties. Emphysema is caused by the protease-antiprotease imbalance when smoking-induced release of neutrophil elastase in the lung is inadequately inhibited by the deficient levels of AAT, the major inhibitor of neutrophil elastase. This protease-antiprotease imbalance leads to proteolytic damage to lung connective tissue (primarily elastic fibers), and the development of panacinar emphysema. AAT replacement therapy, most often applied by weekly intravenous infusions of AAT purified from human plasma, has been used to partially correct the biochemical defect and raise the serum AAT level above a theoretically protective threshold level of 0.8 g/L. A randomized controlled clinical trial was not considered feasible when purified antitrypsin was released for clinical use. However, AAT replacement therapy has not yet been proven to be clinically effective in reducing the progression of disease in AAT-deficient patients. There was a suggestion of a slower progression of emphysema by computed tomography (CT) scan in a small randomized trial. Two nonrandomized studies comparing AAT-deficient patients already receiving replacement therapy with those not receiving it, and a retrospective study evaluating a decline in FEV(1) before and after replacement therapy, suggested a possible benefit for selected patients. Because of the lack of definitive proof of the clinical effectiveness of AAT replacement therapy and its cost, we recommend reserving AAT replacement therapy for deficient patients with impaired FEV(1) (35-65% of predicted value), who have quit smoking and are on optimal medical therapy but continue to show a rapid decline in FEV(1) after a period of observation of at least 18 months. A randomized placebo-controlled trial using CT scan as the primary outcome measure is required. Screening for AAT deficiency is recommended in patients with chronic irreversible airflow obstruction with atypical features such as early onset of disease or disability in their forties or fifties, or positive family history, and in immediate family members of patients with AAT deficiency.

Genetic Testing↗
PubMed1994

CT of the lung in patients with pulmonary emphysema: diagnosis, quantification, and correlation with pathologic and physiologic findings.

Pulmonary emphysema is a pathologic diagnosis. However, the diagnosis can be made with relative certainty on the basis of clinical and radiologic criteria. The clinical diagnosis of emphysema can be difficult because correlations between results of lung function tests and the extent of emphysema are poor. Additionally, features of other obstructive lung diseases may overlap. From the clinician's standpoint, the main value of differentiating between emphysema and other obstructive diseases of the airways (e.g., asthma and chronic bronchitis) is to (1) establish a prognosis and (2) guide the use of corticosteroid therapy by defining the degree of reversibility that can be expected in patients with limitation in air flow.

Female↗
PubMed1997

Pseudomass due to atelectasis in patients with severe bullous emphysema.

OBJECTIVE: This study describes the atypical presentation of atelectasis as a pseudomass in patients with severe bullous emphysema. MATERIALS AND METHODS: The radiologic studies and clinical records of 11 patients with severe bullous emphysema and mass-like opacities representing atelectatic lung were reviewed. The diagnosis was proven by surgery in nine patients and by follow-up imaging in two patients. RESULTS: Pseudomasses were found primarily in the upper lobes and the right middle lobe (n = 10). Common features included an oblong, lenticular, or triangular shape (n = 8); a sharp interface with aerated lung (n = 9); hyperexpansion of the hemithorax containing the pseudomass (n = 8); a central location abutting the mediastinum (n = 8); and adjacent emphysema (n = 11). CT revealed subsegmental atelectasis in other lobes adjacent to the bullous lung in six patients. In three patients, the pseudomasses were associated with persistent distention of large bullae following spontaneous pneumothoraces. Reexpansion of pseudomasses occurred in seven of the eight patients who underwent resection of bullous lung. CONCLUSION: These pseudomasses most likely result from compression of the lung by adjacent large bullae. The diagnosis should be suspected when central, sharply marginated, mass-like opacities that are oblong, lenticular, or triangular are bordered by severe bullous emphysema.

Diagnosis, Differential↗
PubMed2003

CT findings and temporal course of persistent pulmonary interstitial emphysema in neonates: a multiinstitutional study.

OBJECTIVE: The purpose of this study was to evaluate the CT appearance, management, and temporal course of persistent pulmonary interstitial emphysema in neonates. MATERIALS AND METHODS: Criteria for inclusion in the study group included neonates with a history of prematurity who required ventilation for lung disease, development of hyperexpanded radiolucent lung lesions after typical radiographic findings of pulmonary interstitial emphysema, and CT documentation of lung abnormalities. Radiographs and CT scans were reviewed for the anatomic distribution, appearance, and presence of classic lines or dots within a radiolucent mass. We compared the management (surgical vs nonsurgical) and the temporal course in nonsurgical cases for patients in the United States and patients outside the United States. RESULTS: From seven institutions, we identified 17 patients who had persistent pulmonary interstitial emphysema with CT documentation. On CT, all lesions consisted of hyperexpanded cystic radiolucencies. Distribution was single-lobe in nine patients (left upper lobe, n = 5; left lower lobe, n = 3; right middle lobe, n = 1), multilobar in eight patients, and bilateral in six patients. Fourteen patients (82%) showed the characteristic line-and-dot pattern. All patients were initially treated conservatively; nine eventually underwent surgical resection with confirmation at pathology. Of 10 patients who underwent nonsurgical treatment for at least 1 year, lesions resolved in four patients, decreased in size in three asymptomatic patients, and enlarged in three patients, with eventual resection in two. Surgical resection was performed in 89% (8/9) of patients treated in the United States and in 13% (1/8) of patients treated outside the United States. CONCLUSION: Our study found that 82% of patients with persistent pulmonary interstitial emphysema had characteristic CT findings (central lines and dots surrounded by radiolucency). Although most patients in this series eventually underwent surgical resection, initial treatment can be conservative. The decision to perform surgery may have reflected the local medical culture.

Child, Preschool↗
PubMed1982

Increased content of neutrosoluble collagen and dialyzable hydroxyproline in panacinar emphysema and spontaneous pneumothorax.

Hydroxyproline transfer to an incubation medium was studied in ten emphysematous, nine relapsing pneumothorax, and eight control samples surgically removed from 2 females and 25 males, ranging in age from 17 to 69 years. Total hydroxyproline in the lung pieces, expressed as a fraction of DNA, was not modified. A large increase of dialyzable and nondialyzable hydroxyproline fraction was observed in the incubation medium of biopsies from emphysema dn pneumothorax groups. Although the pneumothorax group had average values between controls and emphysema, some pneumothorax patients exhibited very high content of soluble hydroxyproline, suggesting a common pattern between some relapsing pneumothorax and emphysema. These findings could not be due to extracellular degradation during the processing of the samples since the results were not affected by the presence of protease inhibitors. These observations suggest that individuals with emphysema and pneumothrax have abnormalities in lung collagen structure and/or biosynthesis resulting in increased degradation of this macromolecule.

Adolescent↗
PubMedDate not supplied

Emphysema as a result of involuntary exposure to tobacco smoke: morphometrical study of the rat.

Several attempts have been made to describe the relation that exists between tobacco smoke and emphysema, through different experimental models of the active smoker. Despite the negative effects that involuntarily inhaled tobacco smoke can have on the lung, no experimental model of the passive smoker has been proposed. In this study, an experimental model of the involuntary smoker is described and the following hypothesis proposed: Passive exposure to tobacco smoke produces morphological alterations in the rat lung, which are compatible with emphysema. Emphysema will be considered to have been caused when enlargement of the distal airspaces of the lung and lung tissue destruction are demonstrated. Sixty Wistar rats were used, divided into two groups: a control group and a group that was passively exposed to tobacco smoke for a period of 3 months. A morphometrical study of the lung was performed using a computerized system. To demonstrate enlargement of the distal airspaces of the lung, the following variables were quantified: alveolar chord and mean linear intercept index (Lm); tissue loss was demonstrated by means of the quantification of the variables: tissue density, internal alveolar perimeter (IAP), and wall thickness (WT). The elastic fiber was also quantified. The animals that were exposed to tobacco smoke displayed the following significant alterations (p < .05): an increase of the alveolar chord and of the Lm, a decrease of the IAP, WT, and tissue density, and a loss of the elastic component of the lung. On the basis of these findings, it is concluded that the rats that were exposed in a passive way to tobacco smoke display morphological pulmonary alterations that are compatible with the definition of emphysema.

Animals↗
PubMed1989

Alpha 1-antitrypsin deficiency and augmentation therapy in emphysema.

Since the first description of alpha 1-antitrypsin deficiency as a cause of emphysema in 1963, major strides have been made in understanding the structure and function of this important antiprotease, its role in the defense against emphysema, and in new treatment strategies. In order to elucidate the pathogenesis of alpha 1-antitrypsin-associated emphysema and recent developments in therapy for this disease, this paper considers current understanding of the pathogenesis of emphysema, recent information regarding the structure and function of the molecule, and more recent developments in augmentation therapy. The author also discusses the national registry that has been organized for better understanding of the natural history of alpha 1-antitrypsin deficiency in a relatively unselected population.

Drug Administration Schedule↗
PubMed2005

Role of cathepsin S-dependent epithelial cell apoptosis in IFN-gamma-induced alveolar remodeling and pulmonary emphysema.

Th1/Tc1 inflammation and remodeling responses characterized by tissue atrophy and destruction frequently coexist in human diseases and disorders. However, the mechanisms that are used by Th1/Tc1 cytokines, like IFN-gamma, to induce these responses have not been defined. To elucidate the mechanism(s) of IFN-gamma-induced tissue remodeling and destruction, we characterized the pathway that lung-targeted, transgenic IFN-gamma uses to induce alveolar remodeling in a murine pulmonary emphysema modeling system. In these mice, transgenic IFN-gamma caused epithelial cell DNA injury and apoptosis detectable with TUNEL (Roche) and dual annexin V and propidium iodide staining. These responses were associated with death receptor and mitochondrial apoptosis pathway activation. Importantly, apoptosis inhibition with a caspase inhibitor (N-benzylcarboxy-Val-Ala-Asp-fluoromethyl-ketone) or a null mutation of caspase-3 blocked this DNA injury and apoptosis response and significantly ameliorated IFN-gamma-induced emphysema. These interventions also ameliorated IFN-gamma-induced inflammation and decreased pulmonary protease burden. Selective cathepsin S inhibition and a null mutation of cathepsin S also decreased IFN-gamma-induced DNA injury, apoptosis, emphysema, inflammation, and protease accumulation. These studies demonstrate that cathepsin S-dependent epithelial cell apoptosis is a critical event in the pathogenesis of IFN-gamma-induced alveolar remodeling and emphysema. They also link inflammation, protease/antiprotease alterations, and protease-dependent apoptosis in the pathogenesis of Th1/Tc1 cytokine-induced tissue remodeling and destructive responses.

Animals↗
PubMed1999

[Surgical and functional results after surgical lung volume reduction in 94 patients with severe emphysema].

Lung volume reduction (LVR) is a new surgical approach designed to relieve shortness of breath and improve exercise tolerance in patients with severe lung emphysema. The aim of this study was to analyse surgical results and changes in the lung function, gas exchange, exercise tolerance and degree of dyspnoea until two years after LVR. From June 1994 to September 1997 ninety-four patients (31 women and 63 men, mean age 64 [35-79] years) with severe emphysema (12 with alpha 1-Pi-deficiency) underwent unilateral (n = 24) or bilateral (n = 70) LVR. 92 from 94 patients were extubated immediately after surgery. 30 days mortality was 2.2% (2/94), 90 days 3.3% (3/94) respectively. Most common postoperative complications were pneumonia (n = 15, 16%) and air leakage longer than 7 days (n = 22, 23.4%). One month after surgery there was a significant increase in forced expiratory vital capacity after one second (FEV1 59%) and significant decrease in total lung capacity (TLC 19%) and residual volume (RV 28%). Also significant changes were observed in paO2, paCO2, 6-minute walking distance, dyspnoea score and respiratory muscle function. Two years after LVR lung function tests in patients with smokers emphysema showed the benefit to be maintained (high responders). Patients with alpha 1-Pi-deficiency showed 6 to 12 months after surgery a remarkable deterioration of functional data (low responders). In selected patients with severe emphysema surgical LVR shows significant improved pulmonary function, gas exchange, dyspnoea and walking distance. The results are better after bilateral operation. Patients selection, rehabilitation program and interdisciplinary care resulted in a low operative morbidity and mortality.

Adult↗
PubMed1999

[Quantitative computed tomography of pulmonary emphysema].

Computed tomography, and particularly high-resolution computed tomography, allows a detailed exploration of the pulmonary parenchyma. We discuss here work on the use of this technique in the diagnosis and quantification of pulmonary emphysema. We stress first the subjective quantification then the objective approach based on specific software. We summarize our work which has demonstrated. 1) that the relative surface with density below -950 Hounsfield units and measured on millimetric tomographic slices obtained at the end of maximal inspiration is a valuable measurement of the extent of the macroscopic emphysema and reflects the microscopic emphysema; 2) that subjective quantification overestimates minimally extensive emphysema and shows important intra- and inter-operator variability; 3) that indexes derived from computed tomographic images acquired at the end of expiration reflect more the obstructive syndrome than emphysematous destruction; 4) that age and the size of the lungs influence computed tomographic measurements while hyperinflation appears to have no effect. Finally, we present an example of recent work applying the computed tomographic technique.

Diagnosis, Differential↗
PubMed2000

[The respiratory muscles in emphysema. The effects of thoracic distension].

Besides increasing the work of ventilation, emphysema increases lung volume which in itself has a deleterious effect on the inspiratory muscles. We review here the effects of an acute change in lung volume on the configuration of the rib cage and muscle function. We also discuss the effects of the chronic distension associated with emphysema. The effects produced by changes in muscle length and configuration on the mechanical force and action of inspiratory muscles is detailed with particular focus on the diaphragm and its structural adaptations to experimental emphysema. We also analyze the activation pattern of inspiratory and expiratory muscles during the breathing process in patients with emphysema. Finally, we discuss the effects of single-lung transplantation and reduction surgery on chest distension and improved inspiratory muscle function.

Adaptation, Physiological↗
PubMed2000

[Congenital lobar emphysema in adults].

Due to the severity of respiratory symptoms, congenital lobar emphysema often requires surgical treatment in the early stages of life. Diagnosis of congenital lobar emphysema in adult life is therefore unusual, often presenting with mild symptoms. Diagnostic assessment is therefore of great importance in the treatment of these patients. A case of congenital lobar emphysema in an adult is reported and the diagnostic and therapeutical approach are discussed. The use of new diagnostic techniques such as dynamic RMN and SPET V/Q lung scan may improve the accuracy of the diagnostic evaluation. Pulmonary lobectomy led to marked improvement in respiratory function. Accurate diagnosis and appropriate management of congenital lobar emphysema in adult patients can lead to favourable results.

Adult↗
PubMed2002

Congenital lobar emphysema.

Congenital lobar emphysema is a very rare congenital cystic malformation of the lung that can cause acute respiratory distress in early life. This paper reviews 6 cases of congenital lobar emphysema seen over a period of 10 years. The medical records of children with the diagnosis of congenital lobar emphysema were retrospectively reviewed for age at diagnosis, sex, presenting symptoms, investigations, treatment and outcome. There were 4 males and 2 females, and all of them presented before 6 months of age. Three presented with recurrent chest infection, while the other 3 had acute respiratory distress soon after birth. In all, the diagnosis was confirmed by chest x-ray, and the left upper lobe was affected in all of them. Although congenital lobar emphysema is rare, clinical awareness of this condition is important for early diagnosis and effective surgical treatment.

Female↗
PubMed2002

[The role of transforming growth factor-beta(1) in smoking-induced chronic bronchitis and emphysema in hamsters].

OBJECTIVE: To study the role of transforming growth factor-beta(1) (TGF-beta(1)) in the pathogenesis of chronic bronchitis and emphysema. METHODS: An animal model of chronic bronchitis and emphysema was developed in hamsters by chronic smoke inhalation. The expression of TGF-beta(1) mRNA and protein in the pulmonary tissue was observed. The bronchial epithelia was stimulated with cigarette smoke extract (CSE) in vitro and the expression of TGF-beta(1) was measured. RESULTS: 3 months after smoking, the animals developed chronic bronchitis and emphysema. TGF-beta(1) immunoreactivity in the pulmonary tissue and cultured bronchial epithelia increased significantly as compared to the normal control (2.75 +/- 0.23 vs 0.84 +/- 0.39, P = 0.001 and 2.67 +/- 0.16 vs 0.85 +/- 0.54, P = 0.001). The expression of TGF-beta(1) mRNA was also increased in the animal model (1.28 vs 0.98). CONCLUSIONS: Smoking can induce over-expression of TGF-beta(1) in bronchial epithelia, which may be one of the mechanisms for smoking-induced chronic bronchitis and emphysema.

Animals↗
PubMed2002

[Effect of shenmai injection and aminophylline on small airway smooth muscle cell apoptosis and related gene expression in rats with emphysema].

OBJECTIVE: To investigate the effect of Shenmai Injection (SMI) and aminophylline on small airway smooth muscle cell (SASMC) apoptosis and the Fas/FasL expression in the papain induced emphysema model rats. METHODS: Emphysema model in rat was established by a single intratracheal instillation of papain. Apoptosis and Fas/FasL expression of SASMC were examined by immunohistochemical SABC and TUNEL assay at 1, 3, 5, 7, 15 and 30 days after modelling, and the effect of SMI and aminophylline on them were observed. RESULTS: Fas, FasL expressions in normal SASMC were very low with a positive rate of (2.31 +/- 0.05)% and (1.28 +/- 0.47)% respectively. After papain instillation, the positive rates increased along with the prolonging of instillation time. SMI showed an inhibition on SASMC Fas and FasL expression but aminophylline didn't show. SASMC apoptosis was very low in normal rats with a rate of (0.87 +/- 0.32)%, it also raised after papain instillation and increased progressively along with the instillation time. SMI treatment could lower the apoptosis rate but aminophylline couldn't. CONCLUSION: Fas and FasL participated the SASMC apoptosis modulation in emphysema formation. SMI shows a definite treatment effect on emphysema by influencing the Fas and FasL protein expression and reducing SASMC apoptosis through inhibiting the release of inflammatory mediator.

Aminophylline↗