Aaron R Casha1, Alexander Manché2, Liberato Camilleri3, Ruben Gatt4, Krzysztof Dudek5, Michael Pace-Bardon6, Marilyn Gauci7, Joseph N Grima4. 1. Department of Cardiothoracic Surgery, Mater Dei Hospital, Malta; Department of Anatomy, Faculty of Medicine, University of Malta, Malta. Electronic address: aaron.casha@um.edu.mt. 2. Department of Cardiothoracic Surgery, Mater Dei Hospital, Malta. 3. Department of Operational Research and Statistics, Faculty of Science, University of Malta, Malta. 4. Metamaterials Unit, Faculty of Science, University of Malta, Malta. 5. Department of Physics and Astronomy, Uniwersytet Zielonogórski, Zielona Góra, Poland. 6. Department of Medicine, Mater Dei Hospital, Malta. 7. Department of Anaesthesia, Mater Dei Hospital, Malta.
Abstract
OBJECTIVE: A hypothesis is presented suggesting that the pathogenesis of apical lung disease is due to progression of subclinical congenital apical bullae in people with low Body Mass Index (BMI), a combination present in 15% of the population, due to high pleural stress levels present in the antero-posteriorly flattened chests of these individuals. DESIGN: The hypothesis was tested for validity in two apical lung pathologies with widespread epidemiological literature, namely tuberculosis (TB) and primary spontaneous pneumothorax (PSP), assessing whether the hypothesis could identify high-risk populations, explain exceptional cases like apical lower lobe disease and confirm predictions. RESULTS: The biomechanical hypothesis can explain the high-risk factors of apical location, age, gender and low-BMI build, as well as the occurrence of disease in the apex of the lower lobe, in both TB and PSP patients. A predicted common pathogenesis for apical lung disease was confirmed by the higher-than-expected incidence of concomitant TB and PSP. CONCLUSION: Pleural stress levels depend on chest wall shape, but are highest in the apex of young males with low BMI, leading to growth of congenital bullae that can eventually limit clearance inhaled material, superinfect or burst. This hypothesis suggests that low-dose computerized tomography may be used to screen for TB eradication. This paper is the first to propose a biomechanical mechanism for all apical lung disease pathophysiology.
OBJECTIVE: A hypothesis is presented suggesting that the pathogenesis of apical lung disease is due to progression of subclinical congenital apical bullae in people with low Body Mass Index (BMI), a combination present in 15% of the population, due to high pleural stress levels present in the antero-posteriorly flattened chests of these individuals. DESIGN: The hypothesis was tested for validity in two apical lung pathologies with widespread epidemiological literature, namely tuberculosis (TB) and primary spontaneous pneumothorax (PSP), assessing whether the hypothesis could identify high-risk populations, explain exceptional cases like apical lower lobe disease and confirm predictions. RESULTS: The biomechanical hypothesis can explain the high-risk factors of apical location, age, gender and low-BMI build, as well as the occurrence of disease in the apex of the lower lobe, in both TB and PSPpatients. A predicted common pathogenesis for apical lung disease was confirmed by the higher-than-expected incidence of concomitant TB and PSP. CONCLUSION: Pleural stress levels depend on chest wall shape, but are highest in the apex of young males with low BMI, leading to growth of congenital bullae that can eventually limit clearance inhaled material, superinfect or burst. This hypothesis suggests that low-dose computerized tomography may be used to screen for TB eradication. This paper is the first to propose a biomechanical mechanism for all apical lung disease pathophysiology.