C H A P T E R 1 9
Tuberculosis
CHAPTER OUTLINE
Anatomic Alterations of the Lungs
Primary Tuberculosis
Reactivation Tuberculosis
Disseminated Tuberculosis
Etiology and Epidemiology
Tuberculosis Among Health Care Workers
Diagnosis
Mantoux Tuberculin Skin Test
Acid-Fast Staining
Sputum Culture
QuantiFERON-TB Gold Test
Xpert MTB/RIF Assay
Overview of the Cardiopulmonary Clinical Manifestations Associated With Tuberculosis
General Management of Tuberculosis
Pharmacologic Agents Used to Treat Tuberculosis
Respiratory Care Treatment Protocols
Case Study: Tuberculosis
Self-Assessment Questions
CHAPTER OBJECTIVES
After reading this chapter, you will be able to:
•List the anatomic alterations of the lungs associated with tuberculosis.
•Describe the causes of tuberculosis.
•List the cardiopulmonary clinical manifestations associated with tuberculosis.
•Describe the general management of tuberculosis.
•Describe the clinical strategies and rationales of the SOAP presented in the case study.
•Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.
KEY TERMS
Acid-Fast Bacilli
Acid-Fast Bacteria
Caseous Granuloma
Caseous Lesion
Centers for Disease Control and Prevention (CDC)
Directly Observed Therapy (DOT)
Disseminated Tuberculosis
Dormant Tuberculosis (Latent Tuberculosis)
Ethambutol
Exposure Risk in Health Care Workers
Fluorescent Acid-Fast Stain
Ghon Complex
Ghon Nodules
Granuloma
Hemoptysis
Induration
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Infection Control Measures
Isolation Procedures
Isoniazid (INH)
Mantoux Tuberculin Skin Test
Maliary Tuberculosis
Multidrug-Resistant Tuberculosis (MDR-TB)
Mycobacterium avium
Mycobacterium kansasii
Mycobacterium tuberculosis
Nontuberculous Acid-Fast Mycobacteria
Occupational Safety and Health Administration (OSHA)
Postprimary Tuberculosis
Primary Tuberculosis
Prophylactic Use of Isoniazid
Purified Protein Derivative (PPD)
Pyrazinamide (PZA)
Respiratory Isolation
Respiratory Patient Isolation Procedures
Respiratory Protection Devices
Rifampin
Sputum Smear
Streptomycin
Transmission of Tuberculosis
Treatment Noncompliance
Tubercle
Ziehl-Neelsen Stain
Anatomic Alterations of the Lungs
Tuberculosis (TB) is a contagious chronic bacterial infection that primarily affects the lungs, although it may involve almost any part of the body. Clinically, TB is classified as primary TB, reactivation TB, or disseminated TB.
Primary Tuberculosis
Primary tuberculosis (also called the primary infection stage) follows the patient's first exposure to the TB pathogen, Mycobacterium tuberculosis—a rod-shaped bacterium with a waxy capsule. Primary TB begins when the inhaled bacilli implant in the alveoli. As the bacilli multiply over a 3- to 4-week period, the initial response of the lungs is an inflammatory reaction that is similar to acute pneumonia (Fig. 19.1). In other words, a large influx of polymorphonuclear leukocytes and macrophages moves into the infected area to engulf, but not fully kill, the bacilli. This action also causes the pulmonary capillaries to dilate, the interstitium to fill with fluid, and the alveolar epithelium to swell from the edema fluid. Eventually the alveoli become consolidated (i.e., filled with fluid, polymorphonuclear leukocytes, and macrophages). Clinically, this phase of TB coincides with a positive tuberculin reaction—a positive purified protein derivative (PPD) skin test result (see discussion of diagnosis later in this chapter).
FIGURE 19.1 Tuberculosis. (A) Early primary infection. (B) Cavitation of a caseous tubercle and new primary lesions developing.
(C) Further progression and development of cavitations and new primary infections. Note the subpleural location of some of these lesions. (D) Severe lung destruction caused by tuberculosis.
Unlike in pneumonia, however, the lung tissue that surrounds the infected area slowly produces a protective cell wall called a tubercle, or granuloma. In essence, the tubercles work to encapsulate, or trap, the TB bacilli in a nutshell-like structure (see Fig. 19.1A). Although the initial lung lesions may be difficult to identify on a chest radiograph, the lesions may be seen as small, sharply defined opacities. When detected on a chest radiograph, these initial lung lesions are called Ghon nodules. As the disease progresses, the combination of tubercles and the involvement of the lymph nodes in the hilar region is known as the Ghon complex (Fig. 19.2).
FIGURE 19.2 Ghon complex, typical of pulmonary tuberculosis, consists of a parenchymal focus and hilar lymph node lesions. The detailed section of the diagram (right) shows the typical features of tuberculous granuloma: central caseous necrosis surrounded by epithelioid cells, multinucleated giant cells, and lymphocytes. (From Damjanov, I. [2017]. Pathology for the health
professions [5th ed.]. St. Louis, MO: Elsevier.)
Structurally, a tubercle consists of a central core containing caseous necrosis and TB bacilli (also called caseous lesion or caseous granuloma). The central core is surrounded by enlarged epithelioid macrophages, lymphocytes, and multinucleated giant cells. A tubercle takes about 2 to 10 weeks to form. The function of the tubercle is to contain the TB bacilli, thus preventing the further spread of infectious TB organisms. Unfortunately, the tubercle has the potential to break down occasionally, especially in a patient with a depressed immune system. The patient is potentially contagious at this stage. In most cases however, the TB bacilli are effectively contained within the tubercles.
Once the bacilli are controlled—either by the patient's immunologic defense system (which contains the TB bacilli in a tubercle) or by antituberculosis drugs—the healing process begins. Tissue fibrosis and calcification of the lung parenchyma slowly replace the tubercle. This tissue fibrosis and calcification cause lung tissue retraction and scarring. In some cases, the calcification and fibrosis cause the bronchi to distort and dilate—that is, to develop bronchiectasis.
Finally, when the bacilli are isolated within tubercles and immunity develops, the TB bacilli may remain dormant for months, years, or life. Individuals with dormant TB (also called latent TB) do not feel sick or have any TB-related symptoms. They are still infected with TB but do not have clinically active TB. The only indication of a TB infection is a positive reaction to the tuberculin skin test (Mantoux test, discussed later), or TB blood test, and the finding of possible residual scarring on the chest radiograph. Individuals with dormant (latent) TB are not infectious and cannot spread the TB bacilli to others.
Reactivation Tuberculosis
Reactivation tuberculosis (also called postprimary tuberculosis, reinfection tuberculosis, or secondary tuberculosis) is a term used to describe the reappearance (i.e., signs and symptoms) of TB months or even years after the initial infection
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has been controlled. Even though most patients with primary TB recover completely from a clinical standpoint, it is important to note that live tubercle bacilli can remain dormant for decades. A positive tuberculin reaction generally persists even after the primary infection stage has been controlled. At any time, TB may become reactivated, especially in patients with depressed immune systems. Most reactivation TB cases are associated with the following risk factors:
•Malnourished individuals
•People in institutional housing (e.g., nursing homes, prisons, homeless shelters)
•People living in overcrowded conditions
•Immunosuppressed patients (e.g., organ transplant patients, cancer patients)
•Human immunodeficiency virus (HIV) patients (TB is a leading cause of death in HIV patients)
•Alcohol abuse
If the TB infection is uncontrolled, further growth of the caseous granuloma tubercle develops. The patient progressively experiences more severe symptoms, including violent coughing episodes, greenish or bloody sputum (possibly mixed with TB bacilli), low-grade fever, anorexia, weight loss, extreme fatigue, night sweats, and chest pain. It is this gradual wasting of the body that provided the basis for an earlier name for TB—consumption. The patient is highly contagious at this stage. In severe cases a tubercle cavity may rupture and allow air and infected material to flow into the pleural space or the tracheobronchial tree. Pleural complications are common in TB (see Fig. 19.1C).
Disseminated Tuberculosis
Disseminated tuberculosis (also called extrapulmonary TB, miliary TB, and tuberculosis—disseminated) refers to infection from TB bacilli that escape from a tubercle and travel to other sites throughout the body by means of the bloodstream or lymphatic system. In general, the TB bacilli that gain entrance to the bloodstream usually gather and multiply in portions of the body that have a high tissue oxygen tension. The most common location is the apex of the lungs. Other oxygen-rich areas in the body include the regional lymph nodes, kidneys, long bones, genital tract, brain, and meninges (Fig. 19.3).
FIGURE 19.3 Spread of tuberculosis (TB). TB bacilli can spread through the lymphatics, blood vessels, or bronchi. TB bacillis spread by the blood usually accounts for TB in distal sites, such as the urogenital tract, bone, or the brain. Expectorated bacilli may be swallowed and cause intestinal TB. (From Damjanov, I. [2017]. Pathology for the health professions [5th ed.]. St. Louis, MO: Elsevier.)
Genital TB in males damages the prostate gland, epididymis, seminal vesicles, and testes and in females, the fallopian tubes, ovaries, and uterus. The spine is a frequent site of TB infection, although the hip, knee, wrist, and elbow also can be involved. Tubercular meningitis is caused by an active brain lesion seeding TB bacilli into the meninges. Endobronchial TB may develop via direct extension to the bronchi from an adjacent tubercle cavity or the spread of the TB bacilli via infected sputum.
TB complications include massive hemoptysis, pneumothorax, bronchiectasis, extensive pulmonary destruction, malignancy, and chronic pulmonary aspergillosis. Over time, the TB infection may cause mental deterioration, intelletual disability, blindness, and deafness.
When a large number of bacilli are freed into the bloodstream, the result can be the presence of numerous small tubercles—about the size of a pinhead (1 to 5 mm)—scattered throughout the body. This form of TB is termed miliary TB. Miliary TB may be seen in the lungs, liver, and spleen.
Tuberculosis primarily results in a chronic restrictive pulmonary disorder. The major pathologic or structural changes of the lungs associated with TB (moderate to severe reactivation TB) are as follows:
•Alveolar consolidation
•Alveolar-capillary membrane destruction
•Caseous tubercles or granulomas
•Cavity formation
•Fibrosis and secondary calcification of the lung parenchyma
•Distortion and dilation of the bronchi
•Increased bronchial secretions
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Etiology and Epidemiology
TB is one of the oldest diseases known and remains one of the most widespread diseases in the world. Unmistakable evidence has been provided from mummies dating back to the Stone Age, ancient Egypt, and ancient Peru that TB is a long-lived human disease. In early writings, the disease was variously called “consumption,” “Captain of the Men of Death,” and “white plague.” In the nineteenth century, the disease was named tuberculosis, a term that derives mainly from the tubercle formations found during postmortem examinations of victims of the disease.
According to the Centers for Disease Control and Prevention (CDC), there were 9093 (a rate of 2.8 cases per 100,000 persons) new cases of TB were provisionally reported in the United States in 2017. This provisional TB case count was the lowest in the United States since national TB surveillance began in 1953. In 2015, the most recent CDC data available, 470 deaths were attributed to TB. Minority populations continue to disproportionately bear the burden to TB disease. For example, the incidence rates for racial/ethnic groups in 2016 were:
•American Indians or Alaska Natives: 4.7 TB cases per 100,000 persons
•Asians: 18.0 TB cases per 100,000 persons
•Blacks or African Americans: 4.9 cases per 100,000 persons
•Native Hawaiilans and other Pacific Islanders: 13.9 TB cases per 100,000 persons
•Hispanics or Latinos: 4.5 TB cases per 100.000 persons
•Whites: 0.6 TB cases per 100,000 persons
TB is still very prevalent globally. According to the World Health Organization (WHO) 2017 report, TB is one of the top 10 causes of death worldwide. In 2017, 10 million people fell ill with TB, and 1.6 million died from the disease (including 0.3 million among people with HIV). In 2017, an estimated 1 million children became ill with TB and 230 000 children died of TB (including children with HIV associated TB). TB is a leading killer of HIV-positive people. Multidrug-resistant TB (MDRTB) remains a public health crisis and a health security threat.
WHO estimates that there were 558 000 new cases with resistance to rifampicin – the most effective first-line drug, of which – 82% had MDR-TB (see General Management of Tuberculosis, page 308). Globally, TB incidence is falling at about 2% per year. This needs to accelerate to a 4–5% annual decline to reach the 2020 milestones of the End TB Strategy. An estimated 54 million lives were saved through TB diagnosis and treatment between 2000 and 2017. Ending the TB epidemic by 2030 is among the health targets of the Sustainable Development Goals.
In humans, TB is primarily caused by the bacterium Mycobacterium tuberculosis. The mycobacteria are long, slender, straight, or curved rods. The transmission of tuberculosis is almost exclusively caused by aerosol droplets produced by coughing, sneezing, or laughing of an individual with active TB. This accounts for the use of strict isolation procedures in acutely ill patients hospitalized and suspected of having active TB. In fact, it has been shown that in very fine aerosolized spray droplets (0.5 to 1.0 µm), the TB bacilli can remain suspended in the air for several hours after a cough or sneeze. When inhaled, some of the bacilli may be trapped in the mucus of the nasal passages and removed. The smaller bacilli, however, can easily be inhaled into the bronchioles and alveoli. The TB bacilli are highly aerobic organisms and thrive best in areas of the body with high oxygen tension, especially in the apex of the lung.
Patients with treatment noncompliance are a significant reservoir for the transmission of tuberculosis.
People living in closed small rooms with limited access to sunlight and fresh air are especially at risk. Other possible ways of contracting TB include the ingestion of unpasteurized milk from cattle infected with the TB pathogen (usually Mycobacterium bovis) or, in rare cases, direct inoculation through the skin (e.g., a laboratory accident during a postmortem examination).
Tuberculosis Among Health Care Workers
The CDC and Occupational Safety and Health Administration (OSHA) carefully monitor the exposure risk in health care workers and the incidence. The CDC and OSHA periodically issue guidelines for respiratory protective devices and patient isolation procedures. The risk for TB, without question, is elevated in health care workers and those who work in chronic institutionalized environments such as jails, homeless shelters, and nursing homes. The respiratory therapist who assists in bronchoscopy and performs secretion suctioning or other procedures dealing with the patient who has a tracheotomy has an increased risk for TB exposure.
Diagnosis
Symptoms vary with the severity and the extent of the disease. They can be very misleading. They include persistent cough, hemoptysis, loss of appetite and weight loss, pleuritic chest pain, nights sweats, low-grade fever, and chills. Along with chest radiology, commonly used diagnostic methods for TB include the Mantoux tuberculin skin test, acid-fast bacilli (AFB) sputum cultures, the QuantiFERON-TB Gold (QFT-G) test, and the rapid Xpert MTB/RI assay.
Mantoux Tuberculin Skin Test
The most widely used tuberculin test is the Mantoux test, which consists of an intradermal injection of a small amount of a purified protein derivative (PPD) of the tuberculin bacillus (Fig. 19.4). The skin is then observed for induration (a wheal) after 48 hours and 72 hours, with results interpreted as follows:
FIGURE 19.4 (A) Intradermal injections are used to administer the Mantoux skin test, which consists of an intradermal injection of a small amount of a purified protein derivative (PPD) of the tuberculin bacillus. An induration of 10 mm or greater is considered positive. A positive reaction is fairly sound evidence of recent or past infection or disease. (B) Positive tuberculin skin
test. (A, From Bonewit-West, K., Hunt, S., & Applegate, E. [2016]. Today's medical assistant [3rd ed.]. St. Louis, MO: Elsevier. B, From Helbert, M. [2017]. Immunology for medical students [3rd ed.]. Philadelphia, PA: Elsevier.)
•An induration less than 5 mm is a negative result.
•An induration of 5 to 9 mm is considered suspicious, and retesting is required.
•An induration of 10 mm or greater is considered a positive result. A positive reaction is fairly sound evidence of recent or past infection or of active disease.
It should be stressed, however, that a positive reaction does not necessarily confirm that a patient has active TB, but only that the patient has been exposed to the bacillus and has developed cell-mediated immunity to it (i.e., latent TB).
Acid-Fast Staining
Because the M. tuberculosis organism has an unusual, waxy coating on the cell surface, which makes the cells impervious to staining, an acid-fast bacteria test (also called a sputum smear) is performed instead. Several variations of the acidfast stain are currently in use. The frequently used Ziehl-Neelsen stain reveals bright red acid-fast bacilli (AFB) against a blue background (Fig. 19.5A). Another popular technique involves a fluorescent acid-fast stain that reveals luminescent yellow-green bacilli against a dark brown background. The fluorescent acid-fast stain is becoming the acid-fast test of choice because it is easier to read; the stained organism provides a striking contrast to the background material (see Fig. 19.5B).
FIGURE 19.5 Acid-fast staining techniques. (A) Ziehl-Neelsen staining of Mycobacterium tuberculosis from sputum. The red rods are M. tuberculosis. (B) A fluorescent acid-fast stain of M. tuberculosis from sputum. Organisms appear yellow (fluorescent).
(From Murray, P. R., Rosenthal, K. S., Pfaller, M. A. [2016]. Medical microbiology [8th ed.]. Philadelphia, PA: Elsevier.)
Sputum Culture
Because a variety of nontuberculous strains of Mycobacterium can appear on an AFB smear, a sputum culture is often necessary to differentiate M. tuberculosis from other acid-fast organisms. For example, common nontuberculous acid-
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fast mycobacteria associated with chronic obstructive pulmonary disease (COPD) are Mycobacterium avium and Mycobacterium kansasii. Sputum cultures can also identify drug-resistant bacilli and their sensitivity to antibiotic therapy. M. tuberculosis grows very slowly. It takes up to 6 weeks for colonies to appear in culture. When the TB bacterium was first studied, it was given the misleading prefix Myco, which gave the impression that the TB pathogen was fungal. The bacterium growing in agars appeared as colonies and was similar to fungal colonies (Fig. 19.6). However, they are unrelated; TB is caused by a bacterium and not a fungus.
FIGURE 19.6 Cultural appearance of Mycobacterium tuberculosis. From Centers for Disease Control and Prevention, Office of the Associate Director for Communications, Division of Public Affairs, Public Health Image Library. Retrieved from https://phil.cdc.gov/Details.aspx?pid=4428.
QuantiFERON-TB Gold Test
In 2005 the US Food and Drug Administration (FDA) approved the QFT-G test. The QFT-G test is a whole-blood test used for diagnosing M. tuberculosis infection, including latent TB infection. Samples of the patient's blood are mixed with antigens (substances that can generate an immune response) and controls. The QFT-G test contains synthetic antigens that represent two M. tuberculosis proteins (ESAT-6 and CFP-10). The mixture is then allowed to incubate for 16 to 24 hours. After this period, the mixture is measured for the presence of interferon-gamma (IFN-gamma). In patients infected with M. tuberculosis, the white blood cells will release IFN-gamma when in contact with the TB antigens. An elevated IFN-gamma level is diagnostic of TB. Additional clinical evaluations, such as AFB stain of the sputum smear and the chest radiograph, are recommended to further support a positive QFT-G finding.
Xpert MTB/RIF Assay
The Xpert MTB/RIF assay simultaneously detects Mycobacterium tuberculosis and rifampin (RIF) resistance directly from the patient's sputum. The test results are back quickly (in under 2 hours), and minimal technical training is required to run the test. In 2010 the WHO recommended Xpert MTB/RIF for use in TB-endemic countries and is monitoring and helping in the coordination of the global roll-out of the technology of this assay.
More than 100 countries are already using the test, and 6.2 million Xpert MTB/RIF cartridges were attained globally in 2015.
Overview of the Cardiopulmonary Clinical Manifestations Associated With Tuberculosis
The following clinical manifestations result from the pathophysiologic mechanisms caused (or activated) by alveolar consolidation (see Fig. 10.8) and increased alveolar-capillary membrane thickness (see Fig. 10.9)—the major anatomic alterations of the lungs associated with tuberculosis (see Fig. 19.1).
Clinical Data Obtained at the Patient's Bedside
The Physical Examination
Vital Signs
Increased Respiratory Rate (Tachypnea)
Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate:
•Stimulation of peripheral chemoreceptors
•Relationship of decreased lung compliance to increased ventilatory rate
•Pain, anxiety, fever
Increased Heart Rate (Pulse) and Blood Pressure
Chest Pain, Decreased Chest Expansion
Cyanosis
Digital Clubbing
Peripheral Edema and Venous Distention
Because polycythemia and cor pulmonale are associated with severe tuberculosis (TB), the following may be seen:
•Distended neck veins
•Pitting edema
•Enlarged and tender liver
Cough, Sputum Production, and Hemoptysis
Chest Assessment Findings
•Increased tactile and vocal fremitus
•Dull percussion note
•Bronchial breath sounds
•Crackles, wheezing
•Pleural friction rub (if process extends to pleural surface)
•Whispered pectoriloquy
Clinical Data Obtained From Laboratory Tests and Special Procedures
Pulmonary Function Test Findings1
Severe and Extensive Cases (Restrictive Lung Pathology)
Forced Expiratory Volume and Flow Rate Findings
FVC |
FEVT |
FEV1/FVC ratio |
FEF25%–75% |
↓ |
N or ↓ |
N or ↑ |
N or ↓ |
FEF50% |
FEF200–1200 |
PEFR |
MVV |
N or ↓ |
N or ↓ |
N or ↓ |
N or ↓ |
Lung Volume and Capacity Findings
VT |
IRV |
ERV |
RV |
|
N or ↓ |
↓ |
↓ |
↓ |
|
VC |
IC |
FRC |
TLC |
RV/TLC ratio |
↓ |
↓ |
↓ |
↓ |
N |
1Pulmonary function test (PFT) findings are usually normal in most cases of TB.
Arterial Blood Gases
Moderate Tuberculosis
Acute Alveolar Hyperventilation With Hypoxemia2 (Acute Respiratory Alkalosis)
pH |
PaCO2 |
|
PaO2 |
SaO2 or SpO2 |
|
|
|
|
|
↑ |
↓ |
↓ |
↓ |
↓ |
|
|
(but normal) |
|
|
2See Fig. 5.2 and Table 5.4 and related discussion for the acute pH, PaCO2, and 
changes associated with acute alveolar hyperventilation.
Extensive Tuberculosis With Pulmonary Fibrosis
Chronic Ventilatory Failure With Hypoxemia3 (Compensated Respiratory Acidosis)
pH |
PaCO2 |
|
PaO2 |
SaO2 or SpO2 |
|
|
|
|
|
N |
↑ |
↑ |
↓ |
↓↓ |
|
|
(significantly) |
|
|
3See Table 5.6 and related discussion for the acute pH, PaCO2, and 
changes associated with acute ventilatory failure.
Acute Ventilatory Changes Superimposed on Chronic Ventilatory Failure4
Because acute ventilatory changes are frequently seen in patients with chronic ventilatory failure, the respiratory therapist must be familiar with and alert for the following two dangerous arterial blood gas findings:
•Acute alveolar hyperventilation superimposed on chronic ventilatory failure, which should further alert the respiratory therapist to record the following important ABG assessment: possible impending acute ventilatory failure
•Acute ventilatory failure (acute hypoventilation) superimposed on chronic ventilatory failure
4See Table 5.7, Table 5.8, and Table 5.9 and related discussion for the pH, PaCO2, and 
changes associated with acute ventilatory changes superimposed on chronic ventilatory failure.
Oxygenation Indices5
Moderate to Severe Stages
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QS/QT |
DO26 |
VO2 |
|
O2ER |
|
|
|
|
|
|
|
↑ |
↓ |
N or ↑7 |
N or ↑7 |
↑ |
↓ |
6The DO2 may be normal in patients who have compensated to the decreased oxygenation status with (1) an increased cardiac output, (2) an increased hemoglobin level, or (3) a combination of both. When the DO2 is normal, the O2ER is usually normal.
7Increased if febrile.
5
, Arterial-venous oxygen difference; DO2, total oxygen delivery; O2ER, oxygen extraction ratio; QS/QT, pulmonary shunt fraction; 
, mixed venous oxygen saturation; VO2, oxygen consumption.
Hemodynamic Indices8
Severe Tuberculosis
CVP |
RAP |
|
PCWP |
CO |
SV |
|
|
|
|
|
|
↑ |
↑ |
↑ |
N |
N |
N |
SVI |
CI |
RVSWI |
LVSWI |
PVR |
SVR |
N |
N |
↑ |
N |
↑ |
N |
8CO, Cardiac output; CVP, central venous pressure; LVSWI, left ventricular stroke work index; 
, mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVSWI, right ventricular stroke work index; SV, stroke volume; SVI, stroke volume index; SVR, systemic vascular resistance.
Abnormal Laboratory Test and Procedure Results
•Positive tuberculosis skin test (PPD)
•Positive sputum acid-fast bacillus (AFB) stain test
•Positive ABF sputum culture
•Positive QuantiFERON-TB Gold Test
Radiologic Findings
Chest Radiograph
•Increased opacity
•Ghon nodule
•Ghon complex
•Cavity formation
•Cavitary lesion containing an air-fluid level (see Fig. 18.11 and Fig. 18.14)
•Pleural effusion
•Calcification and fibrosis
•Retraction of lung segments or lobe
•Right ventricular enlargement
Chest radiography is most valuable in the diagnosis of pulmonary TB. During the initial primary infection stage, peripheral pneumonic infiltrates (Ghon nodules) can be identified. As the disease progresses, the combination of tubercles and involvement of the lymph nodes in the hilar region (the Ghon complex) can be seen. In severe cases, cavity formation and pleural effusion are seen (Fig. 19.7). Healed lesions appear fibrotic or calcified. Retraction of the healed lesions or segments also is revealed on chest radiographs. In patients with postprimary TB of the lungs, lesions involving the apical and posterior segments of the upper lobes are often seen. In disseminated maliary tuberculosis, the lungs may show myriad 2- to 3-mm granulomatous foci. The radiographic result is widespread fine nodules that are uniformly distributed and equal in size (Fig. 19.8). Finally, because right-sided heart failure (cor pulmonale) may develop as a secondary problem during the advanced stages of TB, an enlarged heart may be seen on the chest radiograph.
