Astrocyte

THE RÖNTGEN CLINIC - THE MORPHOLOGIC EVIDENCE
Year
: 2017  |  Volume : 4  |  Issue : 2  |  Page : 75--79

Pulmonary tuberculosis: A collage of radiological portraits


Nishith Kumar1, Yatish Agarwal1, Pranav Ish2, Arpita Gupta3,  
1 Department of Radiodiagnosis, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
2 Department of Pulmonary Medicine, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
3 Department of Pediatrics, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India

Correspondence Address:
Yatish Agarwal
Department of Radiodiagnosis, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi
India

Abstract

For close to a hundred years, diagnostic radiology has been an invaluable ally of physicians engaged in the diagnosis and treatment of various forms of tuberculosis. Over time, its realm has benefited with quantum expansion in imaging technology and emergence of greater understanding of morphological signs, which can play a decisive role in diagnosis, in monitoring the response to treatment, in screening the close contacts of sputum smear positive pulmonary tuberculosis patients, and in guiding thoracic interventions. This photomontage unveils the classic changes of pulmonary manifestations of the disease through its primary and post-primary forms, expressions in an immunocompromised host, and presentations in multidrug-resistant tuberculosis and in nontubercular mycobacterial infection.



How to cite this article:
Kumar N, Agarwal Y, Ish P, Gupta A. Pulmonary tuberculosis: A collage of radiological portraits.Astrocyte 2017;4:75-79


How to cite this URL:
Kumar N, Agarwal Y, Ish P, Gupta A. Pulmonary tuberculosis: A collage of radiological portraits. Astrocyte [serial online] 2017 [cited 2018 Sep 20 ];4:75-79
Available from: http://www.astrocyte.in/text.asp?2017/4/2/75/219477


Full Text



 Introduction



Tuberculosis is caused by Mycobacterium tuberculosis complex with Mycobacterium tuberculosis being the usual culprit in majority of cases. The primary mode of spread of air-borne bacteria is by droplet transmission with involvement of alveolar macrophages by the inhaled bacilli droplets in terminal airspaces of the lung.[1] The probability of infection and manifestation of the disease depends upon virulence of the bacteria and the immune response of the infected individual.[1] Imaging plays an important role in the diagnosis, in monitoring the response to treatment of active tuberculosis, in screening the close contacts of sputum smear positive pulmonary tuberculosis patients and image guided biopsies. Tuberculosis primarily affects the pulmonary system and has been traditionally classified into primary and post-primary tuberculosis.

 Radiological Characteristics of Pulmonary Tuberculosis



Depending upon the prior exposure to the mycobacterium and underlying host immune response, pulmonary tuberculosis is classically divided into a primary and post-primary form, each with corresponding characteristic radiological features. However, both forms may sometimes present with some overlapping features which can make differentiation difficult.

Primary tuberculosis

Classically, primary tuberculosis, especially in the endemic regions, is a disease of childhood, whereas post-primary tuberculosis is a disease of adulthood. Still a most prevalent form in children under 5 years of age, primary tuberculosis has been demonstrating an upward trend among adults largely due to the easy accessibility to treatment globally and appropriate public health measures. However, due to lack of a high index of suspicion, it is often misdiagnosed, especially, in adults. A chest radiograph is often the first and most commonly used diagnostic test, although it may be normal and unrevealing in a minority of cases.[2]

Primary TB can involve the lung parenchyma with consolidation, mediastinal lymph nodes, proximal airways and pleura.[3],[4] The characteristic form of primary TB is often referred to as gangliopulmonary TB which is a combination of mediastinal and/or hilar lymphadenopathy and associated less conspicuous parenchymal abnormality.[3],[4] The primary pulmonary site of infection is termed as Ghon focus or tubercle which is usually a calcified subpleural lesion and often located in middle or lower zones. The combination of Ghon focus and ipsilateral calcified hilar node is termed as Ranke complex.[4],[5],[6]

Mediastinal lymphadenopathy

Most common imaging manifestation of primary pulmonary tuberculosis, mediastinal lymphadenopathy presents as hypodense peripherally enhancing enlarged mediastinal lymph nodes [Figure 1]a and [Figure 1]b with variable calcification.[3] When this infective lymphadenitis is associated with an extracapsular extension, it produces a conglomeration of the affected nodes. Enlarged mediastinal lymph nodes are present in 83% to 96% of pediatric primary pulmonary tuberculosis as against 10%-43% of adult cases.[3],[7] With anti-tubercular treatment (ATT), the resolution of the nodes is slower in comparison to the prenchymal lesions, and often, partial healing is found in the nodes with calcification.{Figure 1}

Parenchymal disease

Consolidation is the most common parenchymal manifestation of primary pulmonary tuberculosis. Unlike in postprimary tuberculosis, this parenchymal consolidation has no lobar prediction and depicts imaging features similar to other bacterial pneumonias but for a higher incidence of associated necrotic mediastinal lymphadenopathy [Figure 2].[3],[8] Cavitation within the consolidation indicates a progressive primary disease.[3] In a majority of cases, the parenchymal lesions undergo resolution. However, if the resolution is slow or incomplete, a calcified Ghon focus and mass like tuberculoma (s) may persist.{Figure 2}

Pleural effusion and empyema

The prevalence of pleural effusion has a direct correlation with increasing age and close to 25% of adults with primary tuberculosis demonstrate fluid in the pleural cavity.[3],[6] A tubercular pleural effusion is usually a hypersensitivity reaction to tubercular protein making isolation of the bacteria from pleural fluid uncommon. Both USG and CT scan can be used to evaluate such patients and an image guided tap can be carried out. Adenosine deaminase level is elevated in tubercular pleural fluid with lymphocytosis, both being markers of underlying monocyte-macrophage activation.[9]

Tubercular empyema shows pleural effusion in association with thickened enhancing visceral pleura [Figure 3] and is commonly associated with loculations. Untreated, it may communicate with a bronchus resulting in the formation of a bronchopleural fistula [Figure 4]. Sometimes, it may extend exteriorly into the chest wall with the formation of empyema necessitans.[10],[11] Chronic healed complicated pleural effusion presents with calcific pleural thickening which may form a fibrothorax.{Figure 3}{Figure 4}

Airway disease

Tracheobronchial tuberculosis is observed in 10%-20% of patients of pulmonary tuberculosis with TB being the most common cause of bronchial inflammatory stricture.[9] On cross sectional imaging, it usually presents as long segment circumferential mural thickening with irregular luminal narrowing. Common indirect imaging features include segmental and (or) lobar atelectasis, lobar hyperinflation, mucoid impaction or post-obstructive consolidation-collapse.[5],[10],[12]

Miliary tuberculosis

Miliary TB, an acute severe illness results from widespread hematogenous dissemination of TB and occurs in 2%-6% cases of primary tuberculosis. It presents as 1-3 mm diameter small nodules in a random distribution in both lung on chest radiograph/CT [Figure 5].[13],[14] Such patients generally present with hematogenous spread of tuberculosis to other systems like tubercular meningitis which requires other imaging modalities specially MRI to look for meningeal enhancement and basal exudates.{Figure 5}

Postprimary tuberculosis

Postprimary tuberculosis usually results from reactivation of dormant tubercle bacilli (90% cases) but may occur secondary to reinfection with different strain of the bacteria.[14],[15],[16] The most common radiological feature of reactivation pulmonary tuberculosis is focal or patchy consolidation in apical/posterior segment of upper lobes and the superior segments of lower lobes which may be related to increased oxygen tension and relative reduced lymphatic drainage both facilitating bacterial multiplication. Predilection for upper lobe involvement and cavitation are hallmarks of postprimary tuberculosis.

Consolidation and cavitations

Patchy ill-defined consolidation in apical/posterior segment of upper lobes and superior segment of lower lobes is an early and common radiological feature of post primary tuberculosis.[10] Cavitation, a hallmark of post primary tuberculosis is found in 20%-45% cases. Tubercular cavities are quite variable in size, and may possess thick irregular walls during an active infection and thin smooth walls in healed cases [Figure 6]a and [Figure 6]b. It can be complicated by bacterial super infection, mycetoma formation or hemoptysis secondary to adjoining vascular erosion.{Figure 6}

Centrilobular nodules

Liquefaction of the caseous necrosis and infective bronchiolitis with trans-bronchial spread results in centrilobular nodules formation in a branching pattern referred to as tree-in-bud pattern. On CT imaging, they appear as 2-4 mm ill-defined centrilobular nodules in branching pattern with linear thickened branching opacities around the terminal and respiratory bronchioles [Figure 7].[3],[10]{Figure 7}

Tuberculoma formation

Found in about 5% patients with reactivation TB, a tuberculoma appears as a well-defined round to oval nodular lesion 0.5 cm to 4 cm in size with satellite nodules in more than 75% patients [Figure 8]a and [Figure 8]b.[3]{Figure 8}

Signs of active disease

Since the reactivation of tuberculosis is common, it becomes necessary to distinguish between the old healed and active disease lesions. The following morphologic features usually reflect an active disease:[2],[3]

Consolidation in a pulmonary apex or/and superior segment of lower lobes with ipsilateral lymphadenopathyAcinar/centrilobular nodules in a branching pattern (tree-in-bud morphology) with or without bronchopneumonia are a feature of infective bronchiolitis with transbronchial spreadClustered nodules in the upper lobe or superior segment of lower lobes with a usual peribronchial distributionMiliary nodules indicative of hematogenous disseminationThick walled cavities in an appropriate clinical setting. The presence of an air-fluid level in a tubercular cavity usually mirrors a superimposed bacterial or fungal infectionEnlarged peripherally rim-enhancing necrotic mediastinal lymphadenopathy with or without extracapsular extension in the form of conglomeration. While homogenous calcified lymph nodes imply an inactive disease, homogenously enhancing lymph nodes are equivocalUnilateral pleural effusion or empyema

If consolidation is found in the absence of ipsilateral lymphadenopathy, a thick walled cavity is present in the absence of constitutional features in elderly, or bilateral hilar lymphadenopathy or bilateral pleural effusion is found, these features are not specific for pulmonary tuberculosis and such patients require further work-up to exclude nontubercular etiologies.

Currently, no standard guidelines exist regarding the utility of PET-CT in evaluating parenchymal lung lesions. However, it can play a clinching role in differentiating between a possible tubercular lesion and pulmonary malignancy and/or metastasis. In a known parenchymal pulmonary lesion, PET possesses a limited role in differentiating between malignant and nonmalignant lesions. However, since metabolic changes precede morphological ones, PET-CT may play a major role in the assessment of the response to therapy in the future.[2]

When the diagnosis is uncertain, a USG or CT guided needle aspiration and biopsy can help make a pathological diagnosis.

Tuberculosis in immunocompromised host

All immunocompromised patients, whether they be affected with malnutrition, chronic alcoholism, diabetes mellitus, HIV infection, post organ transplant, or those on immunosuppressive therapy fall under an increased risk of developing primary and postprimary tuberculosis.[17] In such cases, the disease is mostly related to reactivation of latent tuberculosis, and clinicoradiologically, it manifests much like primary tuberculosis (i.e. lymphadenopathy and consolidation) with a greater possibility of miliary tuberculosis and non-segmental distribution of multiple cavities than in the immunocompetent host. Severely immunocompromised patients with pulmonary tuberculosis may present with normal chest radiograph in up to 40% cases. Patients with idiopathic pulmonary fibrosis (IPF) have 4 times higher risk of developing tuberculosis than general population with atypical radiological presentation in form of subpleural nodules and segmental/lobar consolidation mimicking bacterial pneumonias.[18]

Multidrug-resistant tuberculosis

The re-emergence of tuberculosis pandemic in association with the rise of HIV-AIDS and development of drug resistant strains is a major public health problem endangering the success of global TB control measures. The imaging features in MDR TB does not significantly vary from drug-sensitive disease except for a higher incidence of multiple cavitatory lesions and features indicative of chronic disease such as bronchiectasis and calcified granulomas.[19]

A strong concordance has been found between the imaging features of MDR TB and the mode of acquisition of drug-resistance. While patients with primary drug resistance — defined as patients who develop MDR TB without having taken anti-TB chemotherapy (ATT) or those who have received the ATT for less than 1 month —commonly present with imaging features of primary tuberculosis pattern in the form of a noncavitatory consolidation or pleural effusion; those patients who develop secondary drug resistance — i.e. MDR TB with ATT of more than one month prior — commonly present with the reactivation pattern and present cavitatory consolidation.[20],[21],[22]

Nontubercular mycobacterial infection

Nontubercular mycobacteria are commonly found in the environment (soil and water). Pulmonary infections are especially common with Mycobacterium avium-intracellulare complex (MAC) and Mycobacterium kansasii. Radiologically, these infections appear as either classic (cavitatory) or bronchiectatic forms.[21] The classic form is similar to postprimary tuberculosis except that it progresses slowly and presents with smaller thin walled cavities. Since sputum smears yield acid fast bacilli in both conditions, a sputum culture is mandatory for a definitive diagnosis.

Non classical presentation typically appears as bronchiectasis and bronchiolitis in the mid to lower zone of the lung. The clinical and radiological features of nontubercular mycobacterial infection in immunocompromised patients are non-specific and overlapping with pulmonary tuberculosis, and thus present a diagnostic dilemma.[22],[23],[24] A poor response to ATT, non-resolution of lesions, chronic indolent course and the evidence of severe immunosuppression are clinical indicators which should encourage evaluation for nontubercular mycobacteria.

 Conclusions



A major public health problem carrying considerable morbidity and mortality, the scourge of tuberculosis offers a major challenge before the global community. The current HIV-AIDS pandemic and emergence of drug resistant tubercular strains has accentuated the quantum of burden. Diagnostic imaging — be it through a good old roentgenogram, CT, USG, and rarely, PET — can play a critical role in the screening, diagnosis and evaluating the treatment response in active tuberculosis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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