Pathogenesis Of Spontaneous Pneumothorax Research Articles

Lung Density Changes With Growth and Inflation

With body growth from childhood, the lungs can enlarge by either increasing the volume of air in the periphery (as would occur with inspiration) or by increasing the number of peripheral acinar units. In the former case, the lung tissue density would decrease with inflation, whereas in the latter case, the lung density would be relatively constant as the lung grows. To address this fundamental structural issue, we measured the CT scan density in human subjects of widely varying size at two different lung volumes. Five hundred one subjects were enrolled in the study. They underwent a chest CT scan at full inspiration and another scan at end expiration. Spirometry, body plethysmography, and diffusing capacity of the lung for carbon monoxide were also measured. There was a strong correlation between the size of the lungs measured at full inspiration on CT scan and the mean lung density (r = -0.72, P = .001). People with larger lungs had significantly lower mean lung density. These density changes among different subjects overlapped the density changes within subjects at different lung volumes. Lung structure in subjects with larger lungs is different from that in subjects with smaller lungs. Tissue volume does not increase in proportion to lung size, as would be required if larger lungs just had more alveoli. These observations suggest that the growth of the lung into adulthood is not accompanied by new alveoli, but rather by enlargement of existing structures. The presence of greater air spaces in larger lungs could impact the occurrence and pathogenesis of spontaneous pneumothorax or COPD.

The Pathogenesis of Spontaneous Pneumothorax in Smokers

The Pathogenesis of Spontaneous Pneumothorax in Smokers

Lung Density Measurements in Spontaneous Pneumothorax Demonstrate Airtrapping

Idiopathic spontaneous pneumothorax (SP) is the result of leakage of air from the lung parenchyma through a ruptured visceral pleura into the pleural cavity. This rupture is thought to be caused by an increased pressure difference between parenchymal airspace and pleural cavity. We hypothesize that rather peripheral airway inflammation leads to obstruction with check valve phenomena and by that to airtrapping in the lung parenchyma, which precedes spontaneous pneumothorax. University hospital. Forty-one matched healthy volunteers (21 smokers and 20 nonsmokers), and 41 patients with SP (21 patients with and 20 patients without bullae) underwent spirometrically controlled high-resolution CT density measurements with automatic contour tracing at 10% and at 90% of vital capacity. Patients with SP showed lower mean lung density (MLD) values and higher percentages of Hounsfield units (HU) below - 900 HU (pixel index [PI]) compared to the healthy volunteers on expiratory scans. This enhanced airtrapping phenomenon is seen in both the SP lung (MLD, p = 002; PI, p = 0.01) and the contralateral lung (MLD, p = 0.009; PI, p = 0.05) compared to the control subjects. The difference with control subjects is independent of smoking behavior and bullae. Peripheral airway obstruction with airtrapping was found, and it is supposed to play an important role in the pathogenesis of spontaneous pneumothorax.

Stature, Lung Height, and Spontaneous Pneumothorax

Relationship between stature and roentgenologically determined lung sizes were examined in 48 patients (mean age = 24.6 +/- 6.2 years) with spontaneous pneumothorax, 46 male patients (mean age = 24.6 +/- 3.8 years) with various diseases not related to the cardiopulmonary system, and 48 healthy male students (mean age = 24.3 +/- 2.2 years). Patients with spontaneous pneumothorax were slender compared to the control groups but the body height was not different. The patients had significantly longer lungs than the controls, although width and depth of the lungs were similar between the three groups. Mean differences for the lung height between patients and healthy students were so small (mean = 1.2-1.7 cm, which is equivalent to 0.3-0.7 cm H2O) that stress alone does not appear to be a major contributor to the pathogenesis of spontaneous pneumothorax.

Spontaneous Pneumothorax: A Study of 105 Cases

SPONTANEOUS pneumothorax is a condition in which air is present outside the lung in the thoracic cavity without obvious portal of entry through the chest wall. The term “pneumothorax” was initially employed by Itard in 1803, when he reported 5 cases, the diagnosis of which was made at autopsy. McDowell in 1856 described the first clear-cut case of spontaneous pneumothorax in an apparently healthy individual. Kjaergaard contributed his monumental work on this subject in 1932. Several hundred cases have since been reported in the literature (exclusive of figures from the military medical services). Many adjectives have been used to describe the pneumothorax. “Benign,” “true,” “real,” “idiopathic,” “simple,” and “spontaneous pneumothorax in apparently healthy individuals” are but a few of the terms. Regardless of terminology, the benign nature of the disease has been stressed by most of the recent investigators. In many medical textbooks the commonest cause of spontaneous pneumothorax is stated to be pulmonary tuberculosis. The purpose of this paper is to present a study of 105 consecutive cases of spontaneous pneumothorax observed at the Columbia-Presbyterian Medical Center, from 1930 to 1947, inclusive, to determine its possible relationship to pulmonary tuberculosis. Pathogenesis The three most important etiological agents in the pathogenesis of spontaneous pneumothorax have been considered to be (1) pulmonary tuberculosis, (2) congenital vesicles, and (3) emphysema. (1) Pulmonary Tuberculosis; Pulmonary tuberculosis has not infrequently been associated with spontaneous pneumothorax. This is apparently based on certain reports in the literature. For example, Fishberg (1932) in his textbook Pulmonary Tuberculosis, remarked that “the consensus of opinion is that the vast majority [of cases of spontaneous pneumothorax] are caused by a tuberculous lesion in the lung or pleura; it is maintained that at least 90 per cent originate thus. The rent in the pleura may be due to softening and consequent perforation of a subpleural tubercle, or to a tear in that membrane caused by tugging of an adhesion. . .. In the writer's opinion probably about 20 per cent of cases of really spontaneous pneumothoraces are not due to tuberculosis.” Rubin stated, in his textbook Diseases of the Chest, that “it was the occasional 'providential' outcome of a spontaneous pneumothorax in the tuberculous that led to the adoption of the procedure as a therapeutic measure.” Kjaergaard (1932) reported 51 cases of spontaneous pneumothorax, and was able to follow 49 of these patients from two to fifteen years. In only one of his cases did pulmonary tuberculosis develop subsequent to the pneumothorax.

A note on the thoracoscope in the treatment of spontaneous pneumothorax

The pathogenesis of spontaneous pneumothorax is outlined. Arguments are adduced in support of performing thoracoscopy and intrapleural pneumolysis as early as possible in these cases Two cases so treated are summarised.