Clinical Manifestations of Pulmonary Tuberculosis

7/28/2019 Clinical Manifestations of Pulmonary Tuberculosis

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Clinical manifestations of pulmonary tuberculosis

Author

Nesli Basgoz, MD Section Editor

C Fordham von Reyn, MD Deputy Editor

Elinor L Baron, MD, DTMH

Last literature review version 17.3: September 2009 | This topic last updated:

February 22, 2005 (More)

INTRODUCTION The lungs are the major site for Mycobacterium tuberculosis

infection. Pulmonary manifestations of tuberculosis (TB) include primary,

reactivation, endobronchial, and lower lung field infection. Complications of TBcan also involve the lung, including hemoptysis, pneumothorax, bronchiectasis

and, in some cases, extensive pulmonary destruction.

The clinical manifestations of pulmonary TB will be reviewed here. The

epidemiology, pathogenesis and treatment of this infection are discussed

separately. (See related topics).

PRIMARY TUBERCULOSIS Primary tuberculosis was considered to be mainly a

disease of childhood until the introduction of effective chemotherapy with

isoniazid in the 1950s. Many studies since that time have shown an increased

frequency in the acquisition of TB in adolescents and adults [1] .

Symptoms and signs The natural history of primary TB was best described in a

prospective study of 517 new tuberculin converters living on the Faroe Islands

off the coast of Norway from 1932 to 1946 [2] . This study included 331 adults

and 186 children, all followed for more than five years. The clinicalmanifestations of primary TB varied substantially in this population, and


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symptoms and signs referable to the lungs were present in only approximately

one-third of patients. Fever was the most common symptom, occurring in 70

percent of 232 patients in whom fever was not a condition for enrollment in the

study. Fever was generally low grade but could be as high as 39C and lasted for

an average of 14 to 21 days. All fever had resolved in 98 percent of patients by

10 weeks.

Symptoms in addition to fever were present only in approximately 25 percent of

patients. Chest pain and pleuritic chest pain were most common. One-half of

patients with pleuritic chest pain had evidence of a pleural effusion. (See

"Tuberculous pleural effusions in non-HIV infected patients" and see

"Tuberculous pleural effusions in HIV-infected patients").

Retrosternal and interscapular dull pain, sometimes worsened by swallowing,

was ascribed to enlarged bronchial lymph nodes. Rarer symptoms were fatigue,

cough, arthralgias and pharyngitis. The physical examination was usually

normal; pulmonary signs included pain to palpation and signs of an effusion.

Radiographic abnormalities The most common abnormality on chest

radiography was hilar adenopathy, occurring in 65 percent [2] . Hilar changes

could be seen as early as one week after skin test conversion and within two

months in all cases. These radiographic findings resolved slowly, often over aperiod of more than one year.

Approximately one-third of the 517 converters developed pleural effusions,

typically within the first three to four months after infection, but occasionally as

late as one year. Pulmonary infiltrates were documented in 27 percent of

patients. Perihilar and right sided infiltrates were the most common, and

ipsilateral hilar enlargement was the rule. While contralateral hilar changes

sometimes were present, only 2 percent of patients had bilateral infiltrates.

Lower and upper lobe infiltrates were observed in 33 and 13 percent of adults,

respectively; 43 percent of adults with infiltrates also had effusions. Most

infiltrates resolved over months to years. However, in 20 patients (15 percent),

the infiltrates progressed within the first year after skin test conversion, so-called

progressive primary TB. The majority of these patients had progression of

disease at the original site, and four developed cavitation.

Other studies, which provide insight into the clinical manifestations of TB, have

focused retrospectively upon patients with culture-proven TB [3-5] . In one seriesfrom Canada, 188 patients were assessed, all of whom were culture positive and


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had abnormal chest radiographs [4] . Thirty patients (18 percent) were classified

clinically as having primary TB. The most common finding was hilar

lymphadenopathy, present in 67 percent. Right middle lobe collapse may

complicate the adenopathy.

Several factors probably favor involvement of the right middle lobe: It is more

densely surrounded by lymph nodes. It has a relatively longer length and smaller

internal caliber. It has a sharper branching angle.

In this retrospective series, pleural effusions were present in 33 percent and

were the sole abnormality in 23 percent [4] . Pulmonary infiltrates were present

in 63 percent of patients; two patients had cavitation and two others evidence of

endobronchial spread.

REACTIVATION TUBERCULOSIS Multiple terms have been used to describe this

stage of TB: chronic TB, postprimary disease, recrudescent TB, endogenous

reinfection, and adult type progressive TB. Reactivation TB represents 90

percent of adult cases in the non-HIV-infected population, and results from

reactivation of a previously dormant focus seeded at the time of the primary

infection. The apical posterior segments of the lung are frequently involved. The

original site of spread may have been previously visible as a small scar called a

Simon focus.

Symptoms The symptoms of reactivation TB have been described mainly in

case series of hospitalized patients in single institutions [6-8] . In these series,

symptoms typically began insidiously and were present for weeks or months

before the diagnosis was made. One-half to two-thirds of patients developed

cough, weight loss and fatigue. Fever and night sweats or night sweats alone

were present in approximately one-half. Chest pain and dyspnea each were

reported in approximately one-third of patients, and hemoptysis in

approximately one-quarter. Many patients had vague or non-specific symptoms;

almost one-third of patients had pulmonary TB diagnosed after an admission for

unrelated complaints [6] .

The cough of TB may be mild initially and may be non-productive or productive

of only scant sputum. Initially, it may be present only in the morning, when

accumulated secretions are expectorated. As the disease progresses, cough

becomes more continuous and productive of yellow or yellow-green sputum,

which is rarely foul-smelling. Frank hemoptysis, due to caseous sloughing or


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endobronchial erosion, typically is present later in the disease and is rarely

massive.

Dyspnea can occur when patients have extensive parenchymal involvement,pleural effusions, or a pneumothorax. Pleuritic chest pain is not common but,

when present, signifies inflammation abutting or invading the pleura, with or

without an effusion. This rarely progresses to frank empyema. Although distinctly

rare in the post-chemotherapy era, patients may present with painful ulcers of

the mouth, tongue, larynx or GI tract which are caused by chronic expectoration

and swallowing of highly infectious secretions.

Presentation in the elderly Many comparative studies have suggested that

pulmonary TB differs in elderly patients compared to younger ones, including alonger duration of symptoms before diagnosis and a lower frequency of

pulmonary and constitutional symptoms. When 12 of these studies were

subjected to a meta-analysis, the time to diagnosis, prevalence of cough, sputum

production, weight loss or fatigue/malaise did not differ significantly between

patients older or younger than 60 years [9] . However, fever, sweats and

hemoptysis were less common in the elderly, and these patients were less likely

to have cavitary disease or a positive purified protein derivative (PPD) skin test.

Elderly patients also more commonly had hypoalbuminemia, leukopenia and

underlying disorders, such as cardiovascular disease, COPD, diabetes,

malignancy, and gastrectomy.

Given the biases inherent in series based upon hospitalized patients, a

population-based study used questionnaires to study the clinical presentation of

TB in prospectively identified confirmed cases among ambulatory patients in Los

Angeles county [10] . The surveyed population of 313 out of a targeted 536

patients (58 percent) was predominantly foreign-born (71 percent); 12 percent

were HIV-infected. When normalized to account for the HIV-infected patients,

fewer patients had cough (48 percent), fever (29 percent), or symptoms for more

than two weeks than in previously published studies. When demographic andclinical features associated with the presence of significant symptoms were

analyzed in a multivariate model, lack of health insurance and a negative PPD

were the only independent predictors of significant symptoms. Patients of Asian

ethnicity tended to lack symptoms.

Despite methodologic limitations, this study suggests that ambulatory patients

with active TB may have even milder and less specific symptoms than those

described in hospitalized patients. It also appears that patients of Asian ethnicity,

a population with a high incidence of TB in the United States, may be even lesslikely to report symptoms than other patients.


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Physical findings Physical findings of pulmonary TB are not specific and usually

are absent in mild or moderate disease. Dullness with decreased fremitus may

indicate pleural thickening or effusion. Rales may be present throughout

inspiration, or may be heard only after a short cough (post-tussive rales). Whenlarge areas of the lung are involved, signs of consolidation associated with open

bronchi, such as whispered pectoriloquy or tubular breath sounds, may be heard.

Distant hollow breath sounds over cavities are called amphoric, after the sound

made by blowing across the mouth of jars used in antiquity (amphora).

Extrapulmonary signs include clubbing and findings localized to other sites of

involvement. (See "Clinical manifestations; diagnosis; and treatment of miliary

tuberculosis").

Laboratory findings Normal laboratory studies are the rule in most pulmonaryTB. Late in the disease, hematologic changes may include normocytic anemia,

leukocytosis, or, more rarely, monocytosis. Hyponatremia may be associated

with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or

rarely with adrenal insufficiency. Hypoalbuminemia and

hypergammaglobulinemia also can occur as late findings.

Radiographic abnormalities Several studies have documented that

reactivation TB typically involves the apical-posterior segments of the upper

lobes (80 to 90 percent of patients), followed in frequency by the superior

segment of the lower lobes and the anterior segment of the upper lobes [6,11-

13] . In recent large series of TB in adults, 70 to 87 percent had the upper lobe

infiltrates typical of reactivation; 19 to 40 percent also had cavities, with visible

air-fluid levels in as many as 20 percent [6,11-13] .

Computed tomographic (CT) scanning is more sensitive than plain chest

radiography for diagnosis, particularly for smaller lesions located in the apex of

the lung [14] . CT scan may show a cavity or centrilobular lesions, nodules andbranching linear densities, sometimes called a "tree in bud" appearance.

The 13 to 30 percent of patients without upper lobe infiltrates are labeled as

having "atypical" radiographic patterns for adult TB [3,15,16] . These

abnormalities included: Hilar adenopathy, sometimes associated with right

middle lobe collapse Infiltrates or cavities in the middle or lower lung zones (see

lower lung field TB below) Pleural effusions Solitary nodules


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These findings are more common in primary TB and probably represent the

known increasing incidence of primary TB in adults, rather than "atypical" forms

of TB.

As many as 5 percent of patients with active TB may present with upper lobe

fibrocalcific changes thought to be indicative of healed primary TB. However, if

such patients have any pulmonary symptoms or lack serial films documenting

stability of the lesion, they should be evaluated for active TB. A normal chest

radiograph is also possible even in active pulmonary TB. As an example, in one

Canadian study of 518 patients with culture-proven pulmonary TB, 25 patients (5

percent) had normal chest x-rays; 23 of these patients had pulmonary symptoms

at the time of the normal radiograph [17] . In this series conducted over a ten-

year period, normal chest x-rays represented fewer than 1 percent of the

radiographs in 1988 to 1989, but increased to 10 percent from 1996 to 1997.

ENDOBRONCHIAL TUBERCULOSIS Endobronchial TB was commonly seen with

both reactivation and primary infection in the prechemotherapy era [18-21] . In a

study in a TB sanatorium in West Virginia, 15 percent of patients had lesions in

the tracheobronchial tree at rigid bronchoscopy and 40 percent at autopsy [18] .

Patients with extensive pulmonary TB, particularly cavitary lesions, were more

likely to have endobronchial disease. It was common to find upper lung

parenchymal or cavitary disease with bronchogenic spread to the lower lung

fields, presumably from pooled infected secretions. At least two mechanisms ofdeveloping endobronchial TB are possible: direct extension to the bronchi from

an adjacent parenchymal focus, usually a cavity, or spread of organisms to the

bronchi via infected sputum from a distant site.

Endobronchial disease in children [22,23] or adults [24,25] with primary infection

is more often associated with impingement of enlarged lymph nodes on the

bronchi. Inflammation results and can be followed by endobronchial ulceration or

even perforation. Complications of endobronchial TB can include obstruction,

atelectasis (with or without secondary infections), bronchiectasis, and tracheal orbronchial stenosis [26] .

Symptoms Symptoms in clinical series include a barking cough, described in

two-thirds of patients, often accompanied by sputum production [24-28] .

Patients rarely develop so-called bronchorrhea, which is production of more than

500 mL per day of sputum [29] . In some cases, caseous material from

endobronchial lesions or calcific material from extension of calcific nodes into the

bronchi can be expectorated, which is known as lithoptysis.


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Wheezing and hemoptysis may also be seen. Lymph node rupture can be

associated with chest pain. Dyspnea, when present, may signal obstruction or

atelectasis. Symptoms may be acute in onset, and be confused with bacterial

pneumonia, asthma [30] , or foreign body aspiration [31] . The clinical

manifestations can also be subacute or chronic, resembling bronchogenic

carcinoma [31] .

Physical findings Diminished breath sounds, rhonchi or wheezing may be

heard. The wheeze is described as low-pitched, constant and always heard over

the same area on the chest wall.

Radiographic abnormalities The most common radiographic finding of

endobronchial TB in adults is an upper lobe infiltrate and cavity with ipsilateralspread to the lower lobe and possibly to the superior segment of the

contralateral lower lobe. Patchy, small lower lobe infiltrates may progress to

confluence or even cavitation. Extensive endobronchial TB can also be

associated with bronchiectasis on CT scan.

When endobronchial TB occurs in patients with primary disease, segmental

atelectasis may be the only finding; atelectasis is more frequent in the right

middle lobe and the anterior segment of the right upper lobe. Because

endobronchial lesions can exist without extensive parenchymal abnormalities, 10to 20 percent of patients may have normal chest radiographs. However, CT

scanning may reveal endobronchial lesions or stenosis.

Diagnosis The diagnosis of endobronchial TB can be made from expectorated

sputum or bronchoscopy similar to other forms of pulmonary TB. (See "Clinical

features and diagnosis of tuberculosis in HIV-infected patients"). While it would

be natural to expect that rates of AFB smear positivity would be high with

extensive endobronchial involvement, rates of 15 to 20 percent have been

reported. This lower rate may be due to bronchial inflammatory tissue which

might prevent expectoration of infected secretions [24,25,28] .

Bronchoscopy of the involved area may show erythematous, vascular and

sometimes ulcerated tissues. Granulation tissue may be bulky or polypoid. Hilar

node rupture may be visible as a mass protruding into the bronchial lumen; with

perforation of the node into the bronchus, caseous or calcific material may be

seen extruding into the lumen. Bronchial stenosis also may be visible [26,32] .

Brushings of the lesions or lavage of the distal airways can increase the


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frequency of positive smears; cultures of this material and sputum are usually

positive.

Treatment Treatment regimens are the same for endobronchial and otherforms of pulmonary TB. (See "Treatment of tuberculosis in HIV-seronegative

patients" and see "Treatment of tuberculosis in HIV-infected patients"). Whether

concomitant steroid therapy is helpful in the treatment of endobronchial disease

is not clear. While acute inflammatory manifestations may improve, steroids

have not been clearly shown to prevent long term complications, such as fibrosis

and stenosis, in controlled studies of lymph node TB in children [25,33,34] .

Repeated dilation, stents, and resection have all been used in the management

of stenotic complications [35-37] . (See "Diagnosis and management of central

airway obstruction").

LOWER LUNG FIELD TUBERCULOSIS Lower lung field TB is defined as disease

located below a line traced across the hila, including the perihilar regions, on a

standard PA and lateral chest x-ray [38] . This uncommon form of the infection

has varied from 2 to 9 percent in incidence in adults, depending upon the patient

population studied [6,38] . As noted above, a number of stages of TB can present

with lower lobe involvement [39-41] : Typical reactivation TB rarely involves the

superior segments of the lower lobes. Endobronchial TB can affect lower lung

fields in both primary infection, especially when adjacent lymph nodes are

involved, and during reactivation, when spread from upper lobe diseasesecondarily infects the lower lung fields. Typical primary tuberculosis. A non-

specific tuberculous pneumonitis, without typical clinical features of either

primary or reactivation TB, can affect the lower lobes. Symptoms in lower lobe

TB resemble reactivation disease and are generally either subacute in onset

(mean of 12 weeks) or chronic (up to six months). Compared to upper lobe TB,

consolidation in the lower lobes tends to be more extensive and homogeneous

[40-42] . Cavitation may be present, and large cavities are reported. This form of

TB is frequently initially misdiagnosed as viral or bacterial pneumonia,

bronchiectasis, or carcinoma.

Elderly patients and those with diabetes, renal or hepatic disease, those

receiving corticosteroids, and those with underlying silicosis appear most at risk

for lower lobe TB. However, many patients have no underlying medical illnesses.

Studies in nursing homes suggest that lower lobe TB may be a manifestation of

tuberculous infection in an older, tuberculin-negative population with significant

underlying diseases or anergy [39] . In some cases, the patients are suspected or

known to have had previous TB, but develop exogenous reinfection, perhaps dueto a loss of demonstrable tissue hypersensitivity.


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TUBERCULOMA Rounded mass lesions can develop during primary infection or

when a focus of reactivation TB becomes encapsulated [42] . These lesions

rarely cavitate. The differential diagnosis of pulmonary coin lesions is extensive.

(See "Diagnostic evaluation and initial management of the solitary pulmonarynodule").

Tuberculomas can be difficult to diagnose, since airway cultures are often

negative. Fine needle aspiration or open lung biopsy may be necessary for

diagnosis.

COMPLICATIONS OF PULMONARY TUBERCULOSIS Pulmonary complications of

TB include hemoptysis, pneumothorax, bronchiectasis and extensive pulmonary

destruction (including pulmonary gangrene).

Hemoptysis Tuberculosis is thought to account for 5 to 15 percent of cases of

hemoptysis in the United States, but an increased proportion in countries with

higher rates of TB [43-45] . Hemoptysis is more common with active

tuberculosis, but may also occur after completion of effective chemotherapy.

Many patients with hemoptysis are smear positive and have cavitary disease,

but the absence of these findings does not preclude hemoptysis.

Bleeding usually is of small volume, appearing as blood-streaked sputum.

Massive hemoptysis is a rare complication of TB today. Prior to effective

chemotherapy when TB sanatoria were common, massive hemoptysis accounted

for approximately 5 percent of deaths from TB. "Rasmussen's aneurysm" causes

massive hemoptysis when TB extends into the adventitia and media of bronchial

arteries, resulting in inflammation and thinning of the vessel wall; this aneurysm

subsequently ruptures into the cavity, producing hemoptysis [46] . While this

mechanism occurs, one autopsy series found Rasmussen's aneurysms in only 6of 80 TB patients with massive hemoptysis [47] . The pulmonary artery,

bronchial arteries without aneurysms, intercostal arteries, and other vessels

supplying the lung also have been found to be sources in cases of massive

hemoptysis due to TB.

Hemoptysis after the completion of therapy for TB only occasionally represents

recurrence of TB. Other explanations for this finding include: residual

bronchiectasis, an aspergilloma or other fungus ball invading an old healed

cavity, a ruptured broncholith that erodes through a bronchial artery, a

carcinoma, or another infectious or inflammatory process.


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Management In most cases, antituberculous chemotherapy, bed rest, and

sedation control bleeding [48] . However, patients with significant TB-related

hemoptysis should undergo rapid evaluation to define the source of bleeding and

facilitate immediate intervention if this is required.

While controlled trials do not exist, several older studies indicate that after one

episode of massive hemoptysis or repeated episodes of severe hemoptysis,

surgical intervention improves survival [49-51] . Bronchial arterial embolization

also has been used as a measure to control bleeding during initial chemotherapy

without surgery, to stabilize patients prior to surgery, or in patients who are not

deemed surgical candidates [52] .

Pneumothorax In the prechemotherapy era, spontaneous pneumothorax was a

frequent and dangerous complication of pulmonary TB [53] . Since the advent of

chemotherapy, spontaneous pneumothorax associated with TB has been

reported in fewer than 1 percent of hospitalized patients [54,55] . However, it

still may be the most common etiology of spontaneous pneumothorax in

countries where TB is endemic.

If cases of TB in which artificial collapse was performed for therapy areeliminated, pneumothorax appears to result from the rupture of a peripheral

cavity or a subpleural caseous focus with liquefaction into the pleural space

[54,55] . Inflammation and the creation of a bronchopleural fistula can result;

such a bronchopleural fistula can seal off spontaneously or persist. In cases of a

permanent seal, the lung may reexpand spontaneously, but more commonly

tube drainage is required.

Factors preventing successful tube drainage and expansion include extensive

pulmonary parenchymal disease with large fistulas, long intervals betweenpneumothorax and chest tube insertion, and the development of an empyema

due to TB and bacterial superinfection. However, successful closure of even

extensive air leaks has been reported after as much as six weeks of tube

drainage accompanied by appropriate antituberculous chemotherapy [56] .

Bronchiectasis Bronchiectasis may develop after primary or reactivation TB

[57-62] . After primary TB, extrinsic compression of a bronchus by enlarged

nodes may cause bronchial dilation distal to the obstruction. There may be no

evidence of parenchymal TB. In reactivation TB, progressive destruction and

fibrosis of lung parenchyma may lead to localized bronchial dilation. If


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endobronchial disease is present, bronchial stenosis may result in distal

bronchiectasis. Bronchiectasis is more frequent in the common sites of

reactivation TB (apical and posterior segments of the upper lobe), but may be

found in other involved areas of the lung. As noted above, bronchiectasis can

also be associated with hemoptysis.

Extensive pulmonary destruction Rarely, TB can cause progressive, extensive

destruction of areas of one or both lungs [63,64] . This is especially in primary

TB, although occasionally lymph node obstruction of the bronchi with a

combination of distal collapse, necrosis, and bacterial superinfection can produce

parenchymal destruction [64] . However, destruction more typically results from

years of chronic reactivation TB, typically in the absence of continuous or

prolonged effective chemotherapy.

Symptoms include progressive dyspnea, hemoptysis and weight loss. In one

series of 18 patients with extensive destruction in one or both lungs, eight died

[63] . Causes of death were massive hemoptysis and respiratory failure,

sometimes in the presence of active TB or superinfection. Radiographically,

patients had large cavities, fibrosis of remaining lung and in some cases, air-fluid

levels at the base of the destroyed lung [63,64] .

The term pulmonary gangrene is used to refer to a more acute destructiveprocess [65] . Patients with this form of TB have rapid progression from a

homogeneous, extensive infiltrate to dense consolidation. There is development

of air-filled cysts which coalesce into cavities. Necrotic lung tissue may be seen

attached to the wall of the cavity. Alternatively, pulmonary gangrene may

resemble an intracavitary clot, fungus ball, or Rasmussen's aneurysm. Pathology

shows arteritis and thrombosis of the vessels supplying the necrotic lung. While

resolution with effective therapy has been reported [66] , mortality usually is

high. In one small series, 75 percent of patients died [65] .

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Clinical Manifestations of Pulmonary Tuberculosis

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