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 TB can 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 clinical manifestations of primary TB varied substantially in this population, and

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 a period 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 series from Canada, 188 patients were assessed, all of whom were culture positive and

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

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 a longer 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 and clinical 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 less likely to report symptoms than other patients.

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). When large 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 pulmonary TB. 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 [6,1113] . 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 and branching 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

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 tenyear 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 of developing 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 or bronchial 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.

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 ipsilateral spread 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, 10 to 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

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

Treatment Treatment regimens are the same for endobronchial and other forms 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 disease secondarily infects the lower lung fields. Typical primary tuberculosis. A nonspecific 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 due to a loss of demonstrable tissue hypersensitivity.

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 pulmonary nodule").

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 6 of 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.

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 are eliminated, 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 between pneumothorax 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

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 destructive process [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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