Clinical diagnosis
Case 274
【Discussion】
When Tbc bacilli infect to human, it is reported that they are repelled by immune system in 90 %, they live through as latent in macrophages in 5 % and they develop and scatter via direct invasion to pulmonary vein or through venous angle through lymphatic channel in 5 % (1, 2). Miliary Tbc occurs in immune compromise situation such as old age, AIDS or during steroid remedy. Miliary nodules are formed by accumulation of immune cells, mainly macrophages. It takes weeks to form miliary nodules after Tbc bacilli infection (1, 2). In our case, he was aged person of 88 with poor nutrient, suffering cardiac disorder and chronic renal disorder, namely in an immune compromised situation.
Silicon sized 0.3 to 3μm is the second atomic factor of earth crust (3, 4). It is contained in rocks including marble stone. Silicosis is one of the pneumoconiosis. Silicon accumulates more predominantly in upper lobes, forming nodules often with calcification rather than in lower lobes. The silicon nodules compose of silicon, macrophages and fibrosis, indicating that macrophages cannot dispose silicon by themselves and need assist with fibroblasts to prevent from silicon activity. The silicon nodules can grow especially at the mediastinum lymph-nodes. Silicon is carried out in flow of lymphatic vessels which has two pathways: subpleural pathway and peri-broncho-vascular bundle. Both pathways reach to mediastinal lymph-node, finally reaching venous angle. Silicon predominantly accumulate in upper lobes rather than lower lobes because ventilation is less decreased from diaphragm motion and perfusion are less decreased because of gravity from earth (3, 4). Then, silicon is more predominantly accumulate in upper lobes rather than lower lobes.
Asbestosis is known to produce plural plaque. Asbestos fiber is needle-shaped and its size is 100μm in length and 30μm in diameter, indicating larger than silicon (3, 5). The size of macrophage which phagocyte foreign body is 20μm, indicating that Asbestos size is too big for mere phagocytic process. Then, it is thought Asbestos is attempted to carry via lymphatic channel but because of its large size and sharp-formed edge, asbestos stay at lymphatic channel in visceral pleura and pass through to parietal pleura with fibrosis by myoblast proliferation, leading formation of plural plaque (5).
When pathogen such as cancer cells or bacteria invade and enter in venous lumen, they flow to systemic circulation. They meet barrier of venous valves, flow into great vessel and reach right ventricle and then carry to the greatest capillary organ of human, lung and thereafter, get caught and stay there (6, 7). Metastatic tumor is usually solid and sometimes it includes low attenuation inside, indicating necrosis. Septic emboli often includes low attenuation, indicating liquid necrosis, cavity. In our case, metastatic solid tumors of lung are shown in Case 4 and cavity formation due to septic emboli, in Case 5. The lesions are more predominant in lower lobes rather than in upper lobes probably because of more perfusion potency in lower lobes than upper lobes.
【Summary】
We presented five cases of miliary Tbc, silicosis, asbestosis, metastatic lung tumor from rectal cancer and septic emboli showing characteristic CT images in each. It is borne in mind that military nodules of military Tbc compose of accumulation of macrophages surrounding Tbc bacilli. Silicosis is predominantly distributed to upper lobe rather than lower lobe probably because upper lobe less perfused and less ventilated when silicon sized 0.3 to 3μm carried in lymphatic vessels. Meanwhile, asbestosis sized 100μm in length and 30μm in diameter, needle like appearance which indicate difficulty to carry in lymphatic and to stay subpleural lymphatic channel and to form pleural plaque from visceral pleura to parietal pleura by piercing pleural space. Metastatic tumor and septic emboli first get caught the largest capillary network, lung except the origin of digestive and visceral organ. Solid tumor often include low attenuation area, named necrosis and septic emboli often include it named cavity are often shown in pulmonary area like Case 4 and Case 5.
【References】
1.Jeong YJ, Lee KS. Pulmonary tuberculosis: upto-date imaging and management. AJR 2008; 191:834–844
2.Houben EN, et al. Interaction of pathogenic mycobacteria with the host immune system. Current Opinion in Microbiology. 2006; 9: 76–85.
3.Kim KI, Kim CW, Lee MK, et al. Imaging of occupational lung disease. RadioGraphics 2001; 21:1371–1391
4.Diseases associated with exposure to silica and nonfibrous silicate minerals. Silicosis and Silicate Disease Committee". Arch. Pathol. Lab. Med. 112 (7): 673–720. July 1988
5.American Thoracic Society (September 2004). "Diagnosis and initial management of nonmalignant diseases related to asbestos". Am. J. Respir. Crit. Care Med. 170 (6): 691–715.
6.Stawicki SP, et al. Septic embolism in the intensive care unit. Int J Crit Illn Inj Sci. 2013 Jan-Mar; 3: 58–63. doi: 10.4103/2229-5151.109423
7.Avery RK, et al. Listeria monocytogenes tricuspid valve endocarditis with septic pulmonary emboli in a liver transplant recipient. Transpl Infect Dis. 1999;1:284–7.
8.Zapol, WM, Snider MT. Pulmonary hypertension in severe acute respiratory failure. N Engl J Med. 1977; 296:476-480.
9.Peña E et al. Pulmonary Hypertension: How the Radiologist Can Help. Radiographics 2012; 30: Chest ImagingFree Access. Published Online:Dec 30 2011https://doi.org/10.1148/rg.321105232
10.Tan RT, et al. Utility of CT scan evaluation for predicting pulmonary hypertension in patients with parenchymal lung disease. Medical College of Wisconsin Lung Transplant Group. Chest 1998;113(5): 1250–1256.
11.Edwards PD, et al. CT measurement of main pulmonary artery diameter. Br J Radiol 1998;71(850):1018–1020.
12. Devaraj A, Hansell DM. Computed tomography signs of pulmonary hypertension: old and new observations. Clin Radiol 2009;64(8):751–760.
2022.8.12