Why does tb affect upper lobes

The elastic fibers within the lung become damaged and replaced by scar tissue, aggravated by exposure to noxious particulates like cigarette smoke that overwhelm the ability of the already meager apical antiprotease defense to prevent elastic fiber damage.

Cycles of destruction, repair and healing lead to fibrobullous lesions and cavity formation in the postero-apical area of the lung around the rib furrows; these then turn into a scarred immunological enclave prone to further disease progression.

The lung is unlike many other organs in that it is not homogeneous in its structure or function but is heterogeneous with regards to its perfusion, ventilation and perfusion-ventilation ratios [ 1 - 4 ], pleural pressure [ 5 ], lymphatic flow [ 6 ], mucociliary clearance [ 7 , 8 ] and pleural mechanical stress [ 9 ].

Much of the heterogeneity of the lungs is due to the effects of gravity [ 10 ], its function as a pressure vessel and of its shape as constrained by the thoracic wall [ 11 , 12 ]. These anatomical and physiological differences affect the lung's responses to various noxious factors that can be extrinsic or intrinsic. These include diverse environmental and congenital factors such as inhalation of injurious gases, particulates and antigens [ 13 - 16 ], infections like tuberculosis TB and aspergillosis [ 17 , 18 ], and genetic disorders like mutations in cystic fibrosis transmembrane conductance regulator CFTR protein and alpha-1 antitrypsin deficiency [ 19 , 20 ].

The aim of this review is to show how various anatomical and physiological features of the upper lobes and apices of the lungs combine to the make this part of the lung more vulnerable to certain disease etiologies, Table 1. In so doing, we aim to demonstrate a common pathophysiological pathway for apical and upper lobe lung disease. Table 1: Classification of upper lobe lung disease by predominant aetiological mechanism. View Table 1. The lungs occupy the pleural cavity.

This cavity is not smooth internally but characterized by ridges caused by the ribs. The most prominent rib ridge is that of the first rib. This may be such a deep furrow that a surgeon might feel a sharp edge on intra-operative palpation [ 21 ]; Figure1.

Computerized tomography scans in coronal and sagittal views show that the apex of the lung sticks out like a thumb from the rest of the lung; Figure 2.

The result is that the apex geometrically has the shape similar to that of a rugby ball or bullet, that is a prolate or elongated spheroidal shape. Figure 1: A,B Anterior and posterior views of moulds of the lung apex showing prominent indentations in the lung parenchyma caused by rib furrows, especially that of the first rib which are deeper posteriorly. Modified after Stephenson [ 21 ].

View Figure 1. Figure 2: Inverted colorized coronal and sagittal reconstructions of a thoracic CT scan showing how the first rib indentation arrow causes the apex of the lung to be very prominent, causing raised levels of pleural stress.

View Figure 2. When the ratio of the height to the base of the apex protruding beyond the first rib reaches 1. Figure 3: Ratios of stress in spheres and in ellipsoids with varying ratios of major a to minor b axes showing axial stress S 1 and circumferential stress S 2. Modified after Fryer [ 22 ]. View Figure 3. When the height to based ratio exceeds 1.

This may result in tearing as the pressure vessel pulls apart. Thinning of the pleura with porosity may also occur [ 23 ].

The tearing or buckling effect results in repair by scarring and fibrosis with repeated cycles of damage and repair that may promote cavity formation [ 11 ]. The negative curvature of the rib grooves further aggravates the issue, resulting in the reversal of the normal surface loads circumferential stresses , leading to tearing in the shoulder areas.

The area most at risk is the posterior aspect of the apex where the first rib furrow is most prominent. Thoracic index is defined as the ratio of anteroposterior and lateral chest diameters.

In the fetus, chest cross-section is circular, although fetal thoracic index exceeds unity in early fetal development [ 24 ]. As children grow, the ribcage drops with gravity, resulting in a change from the horizontal ribs in the cone-shaped fetal chest with a thoracic index of 0.

Gravity acts on ribs to increase their angle of inclination with the horizontal, resulting in drooping of ribs with growth and aging, as the ribs pivot on their costo-vertebral joints. The initial drop in rib angulation in children leads to a drop in thoracic index as children start to walk upright [ 25 ].

The chest wall changes with age [ 26 ]; in particular, the thoracic index increases as the ribs drop outwards and laterally with age. There is a progressive rounding of the thoracic cage with increasing age-related obesity [ 27 ], Figure 4. Chest anteroposterior diameter increases but the lateral diameter remains static [ 28 ].

Presence of centrilobular nodules and tree-in-bud appearance on CT is more sensitive than radiographs in detection of active endobronchial disease. Clustered nodules: Large nodular opacities cm may result due to coalescence of smaller nodules. These usually have irregular margins and are surrounded by tiny satellite nodules. These may appear as nodular patches or masses on CXR. Such nodule clusters, especially in a peribronchial distribution are an indicator of active disease.

Miliary nodules: Small mm , well-defined, randomly distributed nodules that indicate hematogenous spread of infection. These may be inconspicuous on radiographs and evident only on HRCT, which may also show associated septal thickening[ 47 ].

Conglomeration of LNs and obscuration of perinodal fat are also associated with active disease. Viral and fungal infections are less likely to be associated with lymphadenopathy, thus presence of enlarged LNs favors TB[ 49 , 50 ].

Pleural effusion or empyema: Unilateral free effusion and empyema suggest active disease, while isolated pleural thickening with or without calcification indicates healed TB. It may be borne in mind that imaging modalities like CXR and CT serve to detect and localize the disease,[ 34 ] and based on site and morphology of findings, diagnosis of active TB may be suggested. Definitive diagnosis of active TB still requires isolation and identification of M.

Figure 6 demonstrates examples of complications in CTB. When CT features indicate TB but are indeterminate for disease activity, then other criteria like bronchoalveolar lavage [BAL] in case of parenchymal involvement , laboratory parameters erythrocyte sedimentation rate ESR, C-reactive protein CRP, total and differential leukocyte counts TLC, DLC respectively, and Mantoux test , sampling for LNs, thoracocentesis for effusion, clinical response, and follow-up may be employed to resolve the ambiguity.

Imaging features of healed TB. A CXR shows thin-walled cavity in left upper zone. Areas of fibro-bronchiectasis and fibrocalcific lesions are seen in left upper zone, RT upper and mid zones. C CXR shows volume loss in both upper zones with apical pleural thickening, pulled hila, fibro-bronchiectasis, and calcific foci.

D CXR shows fibro-bronchiectasis both upper zones. F CT lung window section in end-stage lung disease shows collapse and bronchiectasis involving the left lung with ipsilateral mediastinal shift and rib crowding.

Imaging features indeterminate for disease activity in CTB. No ipsilateral adenopathy, no cavitation was seen. Note is also made of bronchiectasis and apical pleural thickening.

This node was unchanged in size and morphology after complete course of ATT. Imaging findings in tuberculous complications. B Axial CECT mediastinal window window center 40 HU, width HU shows contrast-filled pseudoaneurym arrow arising from the superior division of RT pulmonary artery Rasmussen aneurysm in the background of fibro-cavitary lesions in both upper lobes. D Coronal CT lung window depicts abnormal communication of pleural space with bronchial tree suggesting a bronchopleural fistula.

Following features are not specific for TB and further work-up to exclude other diagnoses like non-tubercular infections, non-infectious diseases like sarcoidosis, serositis , and even malignancies lymphoma, carcinoma should be undertaken:.

Imaging features of active endobronchial infection in the presence of TB sequelae. These may represent superimposed secondary infection usually pyogenic or reactivation TB. Imaging findings in patients with TB sequelae include bronchovascular distortion, fibro-parenchymal lesions, bronchiectasis, emphysema, and fibro-atelectatic bands indicative of prior infection with scarring.

The former may get colonized by saprophytic fungi aspergilloma and the latter may get calcified. Tuberculomas and small calcified lung nodules also suggest prior infection. Imaging features of healed TB may be detected incidentally or patients may only have some minor symptoms. In such cases, no further imaging is required, especially if a comparison with prior imaging suggests stability of findings, and symptomatic management is done.

However, if the symptoms are severe and refractory, then an initial CT is usually done for comprehensive assessment of lungs, LNs, and pleura. Based on this, definitive management surgery for localized fibro-bronchiectatic disease or palliative measures may be undertaken [bronchial artery embolization BAE for hemoptysis, bronchoscopy-guided or percutaneous antifungal instillation for persistent fungal ball in pre-existing tuberculous cavities].

The initial CT also serves to rule out any reactivation or to detect any superimposed bacterial infection. Secondly, persistent lesions may represent drug-resistant TB, in which case sampling and drug susceptibility testing is recommended.

Appearance of new lesions or reappearance of radio-opacities may represent reactivation TB or superimposed bacterial infections. Thirdly, persistent lesions may suggest the possibility of alternative diagnoses and additional work-up may be undertaken to investigate the patient for the same.

Figure 8 depicts the proposed algorithm. In addition to sputum smear examination, all such patients should be subjected to a CXR, wherever feasible. CXR has been justified as an initial investigation in the evaluation of childhood TB as well. In case of sputum negativity or inability of the patient to produce sputum, CXR serves a pivotal role in guiding management.

If the CXR suggests healed TB, then as delineated in Figure 7 , comparison with prior imaging is desirable to document stability, failing which a CT is usually done to confirm absence of active infection.

In addition to being more sensitive, CECT is especially useful to characterize mediastinal LNs, effusion, and to confirm the parenchymal findings. Based on the CECT findings, the radiologist should categorize the patient into one of the three categories [ Figure 9 ]. Presence of even a single imaging criterion of activity in a suspected case of TB is sufficient to diagnose active disease and warrants ATT.

Demonstration of AFB is desirable and adds supportive evidence, but is not mandatory. Flowchart demonstrating the stratification of patients after CT. Based on CT findings, the patient should be categorized into either active TB, healed TB, or indeterminate for disease activity. In a diagnosed case of CTB, these features help in assessing the disease activity at the time of presentation and during follow-up.

Imaging features indeterminate for disease activity include equivocal radiographic findings, signs of active endobronchial infection in non-predisposed locations, and non-specific evidence of active infection which may suggest superimposed secondary infections. With compliant treatment, clinical improvement is expected within weeks. Follow-up is done at the end of IP and CP. If the patient was sputum-smear positive to begin with, then follow-up is usually done with sputum-smear examination.

However, problems arise when such patients become unable to produce sputum but other symptoms persist. Also, if sputum becomes negative but clinical improvement is discordant, then imaging provides a viable option for response assessment.

Figure 10 depicts the imaging protocol for follow-up of pulmonary and nodal types of CTB. CXR is done at the completion of IP of the treatment regimen. If there is significant resolution of findings or CXR depicts only sequelae of prior infection, then no further imaging is needed even at the end of treatment regimen, provided there is clinical improvement as well.

This is even applicable to those cases where initial disease was evident only on CT. However, if there is scenario 2 at the end of treatment, then the CP may be prolonged depending on clinical and laboratory parameters. In case of no definite response on CXR and absence of clinical improvement scenario 3 , CT may be done to assess disease activity. Non-contrast CT with HRCT reconstructions is sufficient for follow-up of solely parenchymal lesions, but contrast administration is required for follow-up of nodal disease.

IP of ATT may be prolonged in case CT suggests residual active disease or if CT is indeterminate but clinical and laboratory parameters do not suggest any response. If the nodes persist at the completion of treatment regimen, or CECT is equivocal for disease activity, then multiparametric MRI may help.

The latter, being a radiation-free alternative, can be employed instead of CT for follow-up in young patients. It may be noted that residual nodes do not necessarily indicate active disease. Figure 11 demonstrates the imaging follow-up in case of pleural TB. Figure 7 demonstrates the imaging approach to such patients. The same flowchart should be followed for patients incidentally detected to have TB sequelae on imaging and for those clinically suspected to have active TB but were found to have sequelae on CXR.

A comparison with previous radiographs or CT examinations if available is very important. If CXR suggests TB sequelae and there are no new lesions compared with previous imaging, then no further imaging is indicated unless some intervention like BAE is planned. However, if no prior imaging is available, then an initial CECT is usually done to confirm the radiographic findings. CT findings of active infection may suggest a superimposed infection, usually bacterial or reactivation TB.

If the patient presents with significant hemoptysis, then CT thoracic angiography may be done to map out the abnormal arteries in order to plan for BAE. In this review, we have attempted to summarize the criteria to differentiate active TB from sequelae and acknowledge that in conditions where imaging is indeterminate, other parameters be taken into consideration. However, a discussion of non-radiological parameters is beyond the scope of the current review. Further research is, however, required for validation of these recommendations and the same may be revised subject to emergence of new information.

In fact, we expect that these algorithms would enable judicious use of imaging and reduce the number of unnecessary CT examinations in the diagnosis and follow-up of these cases. Source of Support: Nil. Conflict of Interest: None declared. National Center for Biotechnology Information , U. Indian J Radiol Imaging. Author information Copyright and License information Disclaimer. Correspondence: Dr. E-mail: moc. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.

This article has been cited by other articles in PMC. Abstract Chest tuberculosis CTB is a widespread problem, especially in our country where it is one of the leading causes of mortality. Keywords: Chest radiograph, chest tuberculosis pulmonary, nodal and pleural , computed tomography, imaging recommendations, TB active. Background The current guidelines for diagnosis of adult chest tuberculosis TB are based primarily on the demonstration of acid-fast bacilli AFB on sputum microscopy.

Epidemiology: Global Scenario and Indian Perspective TB is a global health problem and the second leading infectious cause of death, after human immunodeficiency virus HIV. Chest TB TB can affect any organ system, although manifestations are most commonly related to the chest. Open in a separate window. Figure 1. Pleural involvement Involvement of the pleura is one of the most common forms of EPTB and is more common in the primary disease.

Complications of CTB Various complications can occur. These include Parenchymal complications Aspergilloma colonization in pre-existing tuberculous cavities. Such patients may also present with hemoptysis as the dominant symptom Destructive lung changes Scar carcinoma - co-existence or secondary development of malignancy Airway complications - tracheobronchial involvement including broncholithiasis and secondary amyloidosis Vascular complications pseudoaneurysms, hypertrophied bronchial arteries, and systemic collaterals , which present with hemoptysis Pleural complications chronic empyema, fibrothorax, bronchopleural fistula, and pneumothorax Mediastinal complications: Mediastinal fibrosis, esophageal involvement in the form of strictures, traction diverticulae, or fistulae , pericarditis, pneumothorax, and spondylodiskitis.

Figure 2 A-E. Does it hurt to breathe? Painful respiration is a symptom of an infection or other medical condition.

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