PULMONARY TUBERCULOSIS WITH BRONCHIECTASIS

Group A

Bambino Mamuaya (1006717810)

Demas Giovani (0906644820)

Mawin Mahen (1006804792)

Case Presentation

Radiology Clinical Rotation

FACULTY OF MEDICINE UNIVERSITAS INDONESIA

RSUPN DR. CIPTO MANGUNKUSUMO

APRIL 2016
Table of Contents
Table of Contents ................................................................................................................................... 2
1. INTRODUCTION .................................................................................................................................. 3
2. CASE ILLUSTRATION ........................................................................................................................... 4
3. LITERATURE REVIEW .......................................................................................................................... 5
3.1 Pulmonary Tuberculosis (PTB) ...................................................................................................... 5
3.2 Bronchiectasis ............................................................................................................................... 5
4. DISCUSSION ...................................................................................................................................... 13
5. CONCLUSION .................................................................................................................................... 14
REFERENCES .......................................................................................................................................... 15
1. INTRODUCTION
2. CASE ILLUSTRATION
Mr. X, a 57-year-old male, came to the hospital due to productive cough since two weeks before
admission. The purulent phlegm was greenish, and sometimes with bright red streaks since one
week ago. There was no night fever or night sweating, but there was decreased appetite and
unintentional loss of body weight. Sometimes the patient felt shortness of breath after coughs,
although there was no dyspnea on effort, paroxysmal nocturnal dyspnea, or orthopnea. The
patient had had lung tuberculosis twice, in which he took anti-tuberculosis medications for six
months and nine months respectively, and was told to be cured on both occasions. Physical
examination results were within normal limits, but the chest x-ray showed cavernous fibrosis
and honeycomb appearance on both upper and lower lobes respectively. The patient was
diagnosed with pulmonary tuberculosis relapse and bronchiectasis.

Figure 1 Chest x-ray showing cavernous fibrosis (blue arrow) and honeycomb appearance (red arrow) in both upper and
lower lobes respectively.
3. LITERATURE REVIEW
3.1 Pulmonary Tuberculosis (PTB)

3.2 Bronchiectasis
Bronchiectasis is defined by the presence of permanent and abnormal dilation of the bronchi,
usually occurs in the context of chronic airway infection causing inflammation. With the
widespread availability of high-resolution computed tomography (HRCT) scanning as the
diagnostic tool of choice, it has been realized that bronchiectasis remains a common and
important cause of respiratory disease.1 It has been estimated that there are at least 110,000
adults in the United States with this condition,2 and the prevalence increased every year from
2000 to 2007 by an annual percentage change of 8.74%.3 Bronchiectasis imposes a significant
burden on patients, i.e. longer hospital stays, more frequent outpatient visits, and more
extensive medical therapy, with a cost of approximately $630 million annually in the United
States. Mortality rate ranged from 10 to 16% over an approximate 4-year observation period.4

Risk Factors

There have been a large number of factors that have been described as causative for
bronchiectasis as shown in Table 1, and generally all have some role in impairing host defence
to infection. The most common cause of bronchiectasis is postinfectious. One acute infectious
episode is thought to result in bronchiectasis, although it has not been definitively demonstrated
in a cohort of patients. A possible mechanism for postinfectious bronchiectasis is a significant
infection in early childhood which causes structural damage to the developing lung and permits
bacterial infection which is not cleared. Over time persistent infection may then result in
bronchiectasis.

A well described sequel to active tuberculosis is the development of bronchiectasis and

subsequent airflow obstruction. The exact incidence is difficult to determine with precision. In
a study of 100 autopsies in 1950, changes of bronchiectasis were described in 46% of cases of
PTB.5 Nowadays, bronchiectasis as a sequel to TB is seen less commonly in the developed
world due to prompt diagnosis and improved access to anti-tuberculous chemotherapy.
Nevertheless, bronchiectasis still complicates active pulmonary TB too frequently in
developing countries. A prospective study from Thailand in 2002 studied all patients diagnosed
with bronchiectasis over a 2 year period from January 1998.6 A history of TB was noted in
32% of the study population with the authors concluding that TB represented the most common
etiological agent responsible for the development of bronchiectasis.

Table 1 Etiologic/risk factors associated with bronchiectasis

Pathology and Pathogenesis

Reid categorized bronchiectasis as having three main phenotypes (Figure 2): 1) tubular
characterized by smooth dilation of the bronchi; 2) varicose in which the bronchi are dilated
with multiple indentations; and 3) cystic in which dilated bronchi terminate in blind ending
sacs.7 The current major form seen on high-resolution computed tomography (HRCT) scanning
is the tubular form of bronchiectasis.
Figure 2 HRCT examples of three forms of bronchiectasis: A) tubular B), varicose, and C) cystic.

The pathophysiologic processes are still not well defined due to the lack of well-established
animal models and due to the its heterogeneous condition where it can be considered the end
result of a variety of different factors. Cole’s vicious cycle model is the generally accepted
explanation for the evolution of bronchiectasis (Figure 3).8 In this model, a predisposed
individual develops a robust inflammatory response to pulmonary infection or tissue injury.
The inflammation that results is partially responsible for the structural damage to the airways,
i.e. marked inflammation of the bronchial wall, principally in the smaller airways, caused the
release of mediators such as proteases which damaged the large airways causing loss of elastin
and other components such as muscle and cartilage which resulted in bronchial dilation (Figure
4). The structural abnormalities allow for mucus stasis, which favors continued chronic
infection and the vicious cycle persists. Over time, retained sputum can cause mucous plugs
and airway obstruction, obliteration, and damage resulting in more advanced bronchiectasis.
The inflammatory response, which involves neutrophils, lymphocytes, and macrophages,
results in further airway destruction and the spread of inflammation beyond the airways
resulting in interstitial pneumonia. How this cycle is initiated may differ according to the
causative disease, but in most cases a circular feedback loop results.
Figure 3 Vicious cycle hypothesis. Host-mediated inflammatory response to foreign material and bacteria in the airway
causes tissue damage resulting in bronchiectasis, which contributes to abnormal mucus clearance and further bacterial
colonization.

Figure 4 Pathologic changes in follicular bronchiectasis as described by Whitwell. A) The first process involves infection of
the small airways. B) This leads to the release of inflammatory mediators such as proteases which damage the large
airways resulting in bronchial dilation and bronchiectasis. C) Infection drives progressive inflammation in the small airways
which become thicker from a combination of cell-mediated inflammatory infiltrate and lymphoid follicles resulting in
obstruction. D) The final process involves the spread of inflammation beyond the airways resulting in interstitial pneumonia.

The characteristic feature of bronchiectasis is airway dilation, but there is a paradoxical finding
where the patients usually have mild to moderate air-flow obstruction with progressive decline
in lung function over time as demonstrated by the loss of forced expiratory volume in one
second (FEV1). Despite dilation of large airways, airflow is obstructed in bronchiectasis due to
the thickening of the bronchial wall of small and medium airways. Since most of the respiratory
tree is composed of medium and small airways, the net effect of the inflammatory process in
bronchiectasis is airflow obstruction.

Clinical Manifestations and Diagnosis

Bronchiectasis should be suspected in any patient with chronic cough and sputum production
or frequent respiratory infections. Additional factors suggesting the diagnosis include the
following: daily sputum production, rhinosinusitis, fatigue, hemoptysis, difficult-to-treat
asthma, nonsmokers diagnosed with COPD, and patients with P. aeruginosa or nontuberculous
mycobacterial (NTM) in their sputum. Although chronic sputum production is the classic
symptom suggesting the diagnosis, patients may have a chronic cough that is nonproductive.
Dyspnea, wheezing, and pleuritic chest pain are also described. HRCT is the diagnostic test of
choice (Figure 5). The main diagnostic features are: 1) internal diameter of a bronchus is wider
than its adjacent pulmonary artery; 2) failure of the bronchi to taper in the periphery of the
chest; and 3) visualization of bronchi in the outer 1–2 cm of the lung fields. Although airway
wall thickening is often present, this radiographic finding is not diagnostic of bronchiectasis,
as it is seen in other airway diseases such as asthma and chronic obstructive pulmonary disease
(COPD).
Figure 5 Radiographic signs of bronchiectasis. A = Bronchus terminating in a cyst; B = lack of bronchial tapering as it travels
to the periphery of the lung; C = signet ring sign (bronchus is larger than the accompanying vessel); D = mucus plug (mucus
completely filling the airway lumen).

Data support the benefit of determining a precise etiology. Shoemark and colleagues noted that
identification of the etiology affected management in 37% of their bronchiectasis cohort. The
first step in evaluation of bronchiectasis is to exclude cystic fibrosis (CF) with two sweat
chloride measurements and gene testing according to CF guidelines. The BTS guidelines for
non-CF bronchiectasis suggest the following evaluation: History to include neonatal
symptoms, infertility, previous pneumonia or viral illness in childhood, gastric aspiration,
asthma, and connective tissue or autoimmune symptoms. Family history is important to
identify genetic causes such as primary ciliary dyskinesia (PCD).

In the absence of PCD and CF, the patient with bronchiectasis should be evaluated for other
etiologies. Sputum should be cultured for bacterial organisms with a separate specimen tested
for acid-fast bacilli. In patients who cannot spontaneously expectorate, sputum induction can
be performed by inhalation of hypertonic saline, a technique that has been shown to be safe
and at least as accurate as bronchoalveolar lavage for isolation of pathogenic organisms in CF.
Bronchoscopy for bronchoalveolar lavage is reserved for patients who (1) are unable to produce
sputum and in whom bacterial infection is suspected, (2) are doing poorly, or (3) whose CT
scan is suggestive of NTM but sputum culture is negative. Magnetic resonance imaging (MRI)
is an underused imaging modality in pulmonary disorders (35) but has been studied in both the
CF and non-CF populations and found to be comparable to CT in detecting airway architecture
distortion without using ionizing radiation, thus thoracic MRI may play a valuable role in the
management of bronchiectasis, especially in pediatric or young adult patients, in whom
sequential exposure to ionizing radiation over the long term is an issue.

Management

A comprehensive approach to bronchiectasis management is important (Figure 4). It is essential

to establish whether an underlying modifiable cause, such as immunoglobulin deficiency or
α1-antitrypsin deficiency, is present. The next step is to initiate an airway clearance regimen
and obtain a sputum sample for bacterial analysis, including acid-fast bacteria. The results of
the sputum culture dictate subsequent choice of antibiotics when indicated. In patients with
frequent exacerbations, chronic macrolide therapy should be considered. Expert opinion
regards exercise, whether part of the patient’s daily routine or in the form of pulmonary
rehabilitation, as integral in management. Overall, the goals of therapy are as follows: (1)
reduce symptoms, (2) improve quality of life, and (3) prevent exacerbations, which are
associated with worse outcomes. Despite long-term, comprehensive management, however,
some patients fail to adequately improve, or demonstrate an inability to tolerate therapy. In
these patients, if the bronchiectasis is localized, referral to a specialized center for surgical
evaluation for lobectomy or segmentectomy may be warranted.
Figure 6 Overview of a comprehensive approach to bronchiectasis management. AAT = α1-antitrypsin; ATS/IDSA =
American Thoracic Society/Infectious Diseases Society of America; IgG = immunoglobulin G; HRCT = high-resolution
computed tomography; NTM = nontuberculous mycobacteria. *A 2-week course is suggested.
4. DISCUSSION
5. CONCLUSION
TB is an infectious disease of an immense burden worldwide, and bronchiectasis is a common
and well-recognized sequalae of PTB. The latter is increasing in prevalence and is associated
with significant morbidity. Management of these patients requires a comprehensive
multimodal therapeutic approach. This approach includes airway clearance, reducing chronic
infection and inflammation, and treatment of exacerbations. Together, these various treatments
work to improve the overall status of the patient with bronchiectasis. Much of the available
information on non-CF bronchiectasis, however, stems from relatively small trials, thus further
stuides are necessary to provide the evidence to guide management decisions and develop new
treatments.
REFERENCES
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Seitz AE, Olivier KN, Adjemian J, Holland SM, Prevots R. Trends in bronchiectasis among Medicare
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McShane PJ, Naureckas ET, Tino G, Strek ME. Non-cystic fibrosis bronchiectasis. Am J Respir Crit Care Med.
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Palwatwichai A, Chaoprasong C, Vattanathum A, et al. Clinical, laboratory findings and microbiologic
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Reid L. Reduction in bronchial subdivisions in bronchiectasis. Thorax. 1950;5:223–247.
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Cole PJ. Inflammation: a two-edged sword—the model of bronchiectasis. Eur J Respir Dis Suppl 1986;147:6–
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