Respiratory System

Chapter 3

Respiratory System


Radiographer Notes

Proper positioning and the correct exposure factors are especially important in radiography of the respiratory system, because to make a precise diagnosis, radiologists must be able to detect subtle changes in pulmonary and vascular structures. Ideally, follow-up studies should be performed with the same exposure factors used to make the initial radiographs. With the same exposure factors, any density changes can be attributed to true pathologic findings rather than to mere technical differences.

All chest radiography should be performed with the patient in full inspiration (inhalation), except when expiration images are used for those few pathologic conditions requiring expiration images. In an ideal image, the upper 10 posterior ribs should be visualized above the diaphragm. Poor expansion of the lungs may cause a normal-sized heart to appear enlarged and makes it difficult to evaluate the lung bases. To obtain a full-inspiration radiograph, the patient should be instructed to take a deep breath, exhale, and inhale again (thus accomplishing maximal inspiration), at which time the exposure should be made. This technique avoids the Valsalva effect, which is a forced expiration against the closed glottis that increases the intrapulmonary pressure. The Valsalva effect results in compression and a large decrease in the size of the heart and adjacent blood vessels, which make it difficult to evaluate heart size and pulmonary vascularity accurately.

The patient must be precisely positioned for chest radiography to ensure symmetry of the lung fields and a true appearance of the heart and pulmonary vasculature. Whenever possible, all chest radiographs should be taken with the patient in the erect position. The only exception is for the patient with a suspected pathologic condition that requires a lateral decubitus position. Although recumbent radiographs may be necessary in immobile or seriously ill patients, they are less than satisfactory because in this position the abdominal contents tend to prevent the diaphragm from descending low enough to permit visualization of well-expanded lung bases or fluid levels. A 72-inch source-to-image receptor distance should be used when possible to minimize magnification of the heart and mediastinal structures. Correct positioning with absence of rotation in the frontal projection can be demonstrated by symmetry of the sternoclavicular joints. The shoulders must be rolled forward (anteriorly) to prevent the scapulas from overlying the lungs. In large-breasted women, it is often necessary to elevate and separate the breasts to allow good visualization of the lung bases. Nipple shadows of both men and women occasionally appear as soft tissue masses. If the nature of these soft tissue masses is unclear, it may be necessary to repeat the examination using small lead markers placed on the nipples. Collimation of the radiograph is required to reduce scattered radiation, although it is essential that both costophrenic angles be visualized. However, the radiographer obtains a diagnostic image, and it is necessary to label the image appropriately.

Radiographs exhibiting a long scale of contrast are necessary to visualize the entire spectrum of densities within the thoracic cavity (including those of the mediastinum, heart, lung markings, and pulmonary vasculature) and the surrounding bony thorax. Most authorities agree that a minimum of 120 kilovolts-peak (kVp) should be used with an appropriate ratio grid for all adult chest radiography. If it is necessary to decrease the overall density, this should be accomplished by reduction of the milliampere seconds (mAs) rather than of the kVp. Decreasing the kVp tends to enhance the bony thorax, which may obscure vascular details and cause under-penetration of the mediastinal structures. In general the density and contrast should be such that the thoracic vertebrae and intervertebral disk spaces are faintly visible through the shadow of the mediastinum without obscuring the lung markings and pulmonary vascularity. Many facilities have advanced from a film-screen imaging system to a digital imaging system, either computed radiography (CR) or direct radiography (DR). With digital systems, density (brightness) and contrast are primarily controlled by the algorithm used to process the image, though the technical factors selected also influence final appearance of the image. When producing radiographs for line placement, the technologist should use the appropriate technical factors to demonstrate the line and possible chest pathology (pneumothorax or hemothorax) that may result from line placement.

Short exposure times (10 msec or less) must be used in chest radiography because longer times may not eliminate the involuntary motion of the heart. Automatic exposure devices are generally recommended, and they help ensure that follow-up studies will have a similar image density. When a digital imaging system is used, the automatic exposure device helps ensure that the exposure index will be within range, thus producing the correct brightness and contrast on the image. An exception is the expiration (exhalation) chest radiograph, which should be exposed with a manual technique because the preset density of an automatic exposure device may cause excessive overexposure of the lungs and thus obscure a small pneumothorax.

Compensatory filters are sometimes needed to overcome the broad range of different tissue densities within the chest. They are especially important to allow good visualization of the mediastinum without overexposing the lungs. The use of compensatory filters generally requires that the radiographic exposure be twice that used when there is no additional filtration.

To demonstrate fluid levels, the patient should be in an erect position for a minimum of 5 minutes (preferably 10 to 15), and a horizontal x-ray beam must be used. Any angulation of the beam prevents a parallel entrance to the air-fluid interface and obscures the fluid level. In some clinical situations (e.g., when there is a small pneumothorax or pleural thickening as opposed to free pleural fluid), it is necessary to use a horizontal beam with the patient placed in the lateral decubitus position.

Certain pathologic conditions of the respiratory system require that the radiographer alter the routine technical factors. Some disorders produce increased tissue density (fluid), which attenuates more of the x-ray beam, whereas others decrease the tissue density of the lungs (hyperaeration) so there is less attenuation by the pulmonary tissue. It is important to remember that these changes may vary for a single disease because the chest structures attenuate more or less of the x-ray beam depending on the stage of the disease process. Unless the radiographer has access to previous images with recorded techniques, the initial exposures should be made with use of a standard technique chart. Adjustments and technical factors can then be made, if necessary, on subsequent images. (See Box 1-1 for a list of the changes in attenuation factors expected in advanced stages of various disease processes.)

Physiology of the respiratory system

The major role of the respiratory system is the oxygenation of blood and the removal of the body’s waste products in the form of carbon dioxide. The respiratory system consists of two separate divisions, the upper tract located outside the thorax and lower tract found within the thoracic cavity (Figure 3-1). The upper respiratory system, which consists of the nasopharynx, oropharynx, and larynx, provides structure for the passage of air into the lower respiratory system. The lower respiratory system, which consists of the trachea, bronchi, and bronchioles, is composed of tubular structures responsible for conducting air from the upper respiratory structures. The smallest unit where gas exchange occurs consists of the terminal bronchiole, alveolar ducts, and alveolar sacs. With the use of the upper and lower respiratory structures, the air from outside the body enters the lungs. The single trachea branches out into two bronchi (one to each lung) at the carina (last segment of the trachea), which in turn branch out into progressively smaller bronchioles to produce a structure termed the bronchial tree because its appearance resembles an inverted tree. The tracheobronchial tree is lined with a mucous membrane (the respiratory epithelium) containing numerous hairlike projections called cilia. During inspiration, the air is moistened and warmed as it enters the lungs. The cilia act as miniature sweepers to prevent dust and foreign particles from reaching the lungs. When the ciliary blanket works correctly, the particles are moved away from the lungs to be coughed up or swallowed. Any damage to the respiratory epithelium and its cilia permits particles (entering with the inspired or inhaled air) to proliferate and produce a disease process.

The vital gas exchange within the lung (called external respiration) takes place within the alveoli, extremely thin-walled sacs surrounded by blood capillaries, which represent the true parenchyma of the lung (see Figure 3-1 inset). Oxygen in the inhaled air diffuses from the alveoli into the blood capillaries, where it attaches to hemoglobin molecules in red blood cells and circulates to the various tissues of the body (called internal respiration). Carbon dioxide, a waste product of cellular metabolism, diffuses in the opposite direction, passing from the blood capillaries into the alveoli and then exiting the body during expiration (or exhalation). Because individual alveoli are extremely small, chest radiographs can demonstrate only a cluster of alveoli and their tiny terminal bronchioles, which are the basic anatomic units of the lung. A cluster of alveoli is termed the acinus.

Respiration is controlled by a center in the medulla at the base of the brain. The level of carbon dioxide in the blood regulates the respiratory center. Even a slight increase in the amount of carbon dioxide in the blood increases the rate and depth of breathing, such as when an individual exercises. The accumulation of waste gases that must be removed from the body (and the body’s need for additional oxygen) causes the respiratory center to stimulate the muscles of respiration—the diaphragm and the intercostal muscles between the ribs. Contraction of the muscles of respiration causes the volume of the chest cavity to increase. This decreases the pressure within the lungs and forces air to move into the lungs through the tracheobronchial tree. As the respiratory muscles relax, the volume of the chest cavity decreases, and air is forced out of the lungs. Special muscles of expiration (abdominal and internal intercostal muscles) may be needed for difficult breathing or in patients with decreased gas exchange, as occurs in emphysema.

Unlike most other organs, the lung has two different blood supplies. The pulmonary circulation is a low-pressure, low-resistance system through which oxygen enters and carbon dioxide exits the circulatory system. The bronchial circulation, which is a part of the high-pressure systemic circulation, supplies oxygenated blood to nourish (or support) the lung tissue itself.

A double-walled membrane consisting of two layers of pleura encases the lungs (Figure 3-2). The visceral pleura is the inner layer that adheres to the lung, whereas the parietal pleura lines the inner chest wall (the thoracic cavity). Between the two layers of pleura is a potential space (pleural space), which normally contains only a small amount of fluid to lubricate the surfaces to prevent friction as the lungs expand and contract. The airtight space between the lungs and the chest wall has a pressure a bit less than that in the lungs. This difference in pressure acts like a vacuum to prevent the lungs from collapsing. An inflammatory or neoplastic process that involves the pleura may produce fluid within the potential space (a pleural effusion).

Internal devices

Endotracheal Tube

A chest radiograph should always be obtained immediately after endotracheal intubation to ensure proper positioning of the tube, because clinical evaluation (bilateral breath sounds, symmetric thoracic expansion, and palpation of the tube in the sternal notch) does not allow detection of the majority of malpositioned tubes. Daily radiographs are usually taken to ensure that the tube has not been inadvertently displaced by the weight of the respiratory apparatus, the patient’s coughing, or other unforeseen events. In addition, imaging permits prompt detection of complications of intubation and barotrauma (positive-pressure breathing), such as pneumothorax and pneumomediastinum.

The relationship between the tip of the tube and the carina (tracheal bifurcation) must be carefully assessed. When the head and neck are in a neutral position, the endotracheal tube tip ideally should be about 5 to 7 cm above the carina (Figure 3-3). With flexion and extension of the neck, the tip of the tube will move about 2 cm caudally and cranially, respectively.

About 10% to 20% of endotracheal tubes require repositioning after insertion. A tube positioned too low usually extends into the right mainstem bronchus, where it eventually leads to atelectasis of the left lung (see Figure 3-76). A tube positioned excessively high or in the esophagus causes the inspired air to enter the stomach, causing severe gastric dilatation and a high likelihood of regurgitation of gastric contents and aspiration pneumonia.

Central Venous Catheters

Central venous catheters inserted into the subclavian vein or a more peripheral vein in the upper extremity are extremely useful for measurement of the central venous pressure (CVP) and for providing a conduit for the rapid infusion of fluid or chronic hyperalimentation. So that the CVP may be correctly measured, the catheter must be located within the true central venous system, beyond all the valves that interfere with direct transmission of right atrial pressure to the catheter. The optimal location is where the brachiocephalic veins join to form the superior vena cava (medial to the anterior border of the first rib on chest radiographs) or within the superior vena cava itself.

Because up to one third of CVP catheters are initially inserted incorrectly, the position of the catheter should be confirmed by a chest radiograph. The most common aberrant location of a CVP catheter is the internal jugular vein (Figure 3-4). CVP catheters that extend to the right atrium are associated with an increased risk of cardiac arrhythmias and even perforation. Extension of the catheter into the hepatic veins may result in the infusion of potentially toxic substances (some antibiotics and hypertonic alimentation solutions) directly into the liver. Even after successful placement, CVP catheters may change position as a result of patient motion or medical manipulation. Therefore, periodic radiographic confirmation of the catheter position is often recommended.

The anatomy of the subclavian region may lead to complications when a central catheter is introduced via the subclavian vein. Because the pleura covering the apex of the lung lies just deep to the subclavian vein, a pneumothorax may develop. This problem may be difficult to detect clinically, and thus a chest radiograph (if possible with the patient in an upright position and in expiration) should be obtained whenever insertion of a subclavian catheter has been attempted. Another complication is perivascular CVP catheter placement, which may result in ectopic infusion of fluid into the mediastinum or pleural space. This diagnosis should be suggested if there is rapid development of mediastinal widening or pleural effusion after CVP catheter insertion (Figure 3-5). Other complications include inadvertent puncture of the subclavian artery, air embolism, and injury to the phrenic nerve.

The peripherally inserted central catheter (PICC) has become the long-term venous access device used for home therapy and for patients undergoing chemotherapy (Figure 3-6).

Catheter breakage and embolization can result from laceration of the catheter by the needle used to insert it, fracture at a point of stress, or detachment of the catheter from its hub. The catheter fragment may lodge in the vena cava, in the right side of the heart, or in branches of the pulmonary artery (Figure 3-7). Adverse results include thrombosis, infection, and perforation.

Swan-Ganz Catheter

The flow-directed Swan-Ganz catheter consists of a central channel for measuring pulmonary capillary wedge (PCW) pressure and a second, smaller channel connected to an inflatable balloon at the catheter tip. Cardiac output and CVP can also be measured using the Swan-Ganz catheter. It can be inserted at the bedside and floated to the pulmonary artery without the need for fluoroscopic monitoring.

Ideally the catheter is positioned so that it lies within the right or left main pulmonary artery. Inflating the balloon causes the catheter to float downstream into a wedge position; deflating the balloon permits the catheter to recoil into the central pulmonary artery. Unlike standard intravenous catheters, the Swan-Ganz catheter has a radiopaque strip down its center. Radiographically the tip of the tube is visualized within the borders of the mediastinum when properly placed; this would substantially decrease the likelihood of occlusion of the distal pulmonary vessel.

The most common complication associated with the use of a Swan-Ganz catheter is pulmonary infarction distal to the catheter tip. Infarction may result from occlusion of a pulmonary artery by the catheter itself (if it is wedged in a too peripheral vessel) or from clot formation in or about the catheter. Pulmonary infarction appears as a patchy air-space consolidation involving the area of the lung supplied by the pulmonary artery in which the catheter lies. The appropriate treatment is simply removal of the Swan-Ganz catheter; systemic heparinization is not required once this source of emboli or obstruction has been removed.

Transvenous Cardiac Pacemakers

Transvenous endocardiac pacing is the method of choice for maintaining cardiac rhythm in patients with heart block or bradyarrhythmias. Radiographic evaluation plays an important role in the initial placement of a pacemaker and in the detection of any subsequent complications. An overexposed image can demonstrate both the generator (for permanent pacemakers) and the course of the electrodes.

Ideally, the tip of the pacemaker should be positioned at the apex of the right ventricle. One common aberrant location is the coronary sinus. On a frontal radiograph, the tip often appears to be well positioned. A lateral projection is required to show that the tip is directly posterior in the coronary sinus, rather than in its proper position anterior in the right ventricle.

Although electrode fractures have become less common because of the development of new alloys, they are still a significant cause of pacing failure (Figure 3-8). The usual sites of fracture are near the pulse generator, at sharp bends in the wires, and at the point where the electrodes are inserted into the epicardium. Although most electrode fractures are easily detected on routine chest radiographs, some subtle fractures may be demonstrated only on oblique views or at fluoroscopy.

Perforation of the myocardium by an intravenous electrode usually occurs at the time of insertion or during the first few days thereafter. Perforation should be suspected when the pacemaker fails to sense or elicit a ventricular response. Plain radiographs show the electrode tip lying outside the right ventricular cavity (Figure 3-9).

Congenital/hereditary diseases

Cystic Fibrosis

Cystic fibrosis (mucoviscidosis) is a hereditary disease characterized by the secretion of excessively viscous mucus by all the exocrine glands; it is caused by a defective gene in the middle of chromosome 7. Cystic fibrosis is the most common clinically important genetic disorder among white children. This disorder also affects the pancreas and digestive system. However, 90% of the morbidity and mortality related to cystic fibrosis occurs as a result of respiratory involvement.

In the lungs, thick mucus secreted by mucosa in the trachea and bronchi blocks the air passages. The thick mucus is the result of an imbalance of sodium and chloride production and reabsorption. These mucous plugs lead to focal areas of lung collapse. Recurrent pulmonary infections are common because bacteria that are normally carried away by mucosal secretions adhere to the sticky mucus produced in this condition. Because of the recurring nature of the disease, by age 10 years many children have widespread bronchiectasis with the formation of large cysts and abscesses. In the pancreas, blockage of the ducts by mucous plugs prevents pancreatic enzymes from entering the duodenum. This process impairs the digestion of fat, resulting in failure of the child to gain weight and the production of large, bulky, foul-smelling stools. In about 10% of newborns with cystic fibrosis, the thick mucus causes obstruction of the small bowel (meconium ileus) (Figure 3-10). Bowel perforation with subsequent fatal peritonitis may occur.

Involvement of the sweat glands in cystic fibrosis causes the affected child to perspire excessively. The perspiration excess leads to a loss of large amounts of salt (sodium, potassium, and chloride), two to three times the normal amount. Patients are therefore extremely susceptible to heat exhaustion in hot weather. The presence of excessive chloride on the skin is the basis for the “sweat test,” a simple and reliable test for cystic fibrosis.


Patient well-being depends on the use of prophylactic antibiotics, chest physiotherapy (percussions), and improved airflow. Prophylactic antibiotics reduce the risk of lung infections that may cause permanent lung damage or bronchiectasis. Chest physiotherapy (hand tapping against the chest) prevents lungs from filling with viscous mucus by keeping the mucus moving. Improved airflow depends on the use of bronchodilators. Currently to help control pulmonary infections, administered by inhalation is recombinant human deoxyribonuclease (DNase), an enzyme that digests the DNA of bacterial and inflammatory cells in the lungs. The newest research trials focus on methods to control the production and reabsorption of sodium and chloride. In the future, gene therapy will be a viable alternative for patients with cystic fibrosis.

Hyaline Membrane Disease

Hyaline membrane disease, also known as idiopathic respiratory distress syndrome (IRDS), is one of the most common causes of respiratory distress in the newborn. It occurs primarily in premature infants, especially those who have diabetic mothers or who have been delivered by cesarean section. Hypoxia and increasing respiratory distress may not be immediately evident at birth but almost always appear within 6 hours of delivery.

The progressive underaeration of the lungs in hyaline membrane disease results from a lack of surfactant and immature lungs. Surfactant consists of a mixture of lipids, proteins, and carbohydrates that creates a high surface tension, requiring less force to inflate and maintain the alveoli. Normally the alveolar cell walls produce lipoprotein, which maintains the surface tension within the alveoli. This tension permits the alveoli to remain inflated so that atelectasis does not occur. The disease process results from surfactant deficiency caused by cell immaturity or birth trauma.


New treatment advances for this disease include the use of an artificial surfactant, which offers the best therapy to reduce morbidity and mortality from this disease process. The artificial surfactant is administered into the airways via a saline solution.

The treatment of hyaline membrane disease includes the use of positive-pressure ventilators that pump air (often with high concentrations of oxygen) into the lungs through an endotracheal tube. The positive-pressure ventilator ensures satisfactory levels of tissue oxygenation. The high ventilator pressure may cause leakage of air from overinflated alveoli or small terminal bronchioles, leading to interstitial emphysema, pneumothorax, and pneumopericardium, all of which further decrease the expansion of the lungs.

Inflammatory disorders of the upper respiratory system


Croup is primarily a viral infection of young children that produces inflammatory obstructive swelling localized to the subglottic portion of the trachea. The edema causes inspiratory stridor or a barking cough, depending on the degree of laryngeal obstruction.


Acute infections of the epiglottis, most commonly caused by Haemophilus influenzae in children, cause thickening of epiglottic tissue and the surrounding pharyngeal structures. The incidence of epiglottitis has decreased dramatically since the inception of the Haemophilus influenzae type B (HiB) vaccine as a routine childhood immunization.

Inflammatory disorders of the lower respiratory system


Acute pneumonia is an inflammation of the lung that can be caused by a variety of organisms, most commonly bacteria and viruses. Regardless of the cause, pneumonias tend to produce one of three basic radiographic patterns.

Alveolar Pneumonia

Alveolar, or air-space, pneumonia, exemplified by pneumococcal pneumonia, is produced by an organism that causes an inflammatory exudate that replaces air in the alveoli, so that the affected part of the lung is no longer air containing but rather appears solid, or radiopaque (Figure 3-15). The inflammation spreads from one alveolus to the next by way of communicating channels, and it may involve pulmonary segments or an entire lobe (lobar pneumonia).

Radiographic Appearance: Consolidation of the lung parenchyma with little or no involvement of the airways produces the characteristic air bronchogram sign (Figure 3-16). The sharp contrast between air within the bronchial tree and the surrounding airless lung parenchyma permits the normally invisible bronchial air column to be seen radiographically. The appearance of an air bronchogram requires the presence of air within the bronchial tree, which suggests that the bronchus is not completely occluded at its origin. Presence of an air bronchogram excludes the diagnosis of a pleural or mediastinal lesion because there are no bronchi in these regions. Because air in the alveoli is replaced by an equal or almost equal quantity of inflammatory exudate and because the airways leading to the affected portions of the lung remain open, there is no evidence of volume loss in alveolar pneumonia.


Bronchopneumonia, typified by staphylococcal infection, is primarily an inflammation that originates in the bronchi or the bronchiolar mucosa and spreads to adjacent alveoli. Because alveolar spread of the infection in the peripheral air spaces is minimal, the inflammation tends to produce small patches of consolidation. Bronchial inflammation causing airway obstruction leads to atelectasis with loss of lung volume.

Interstitial Pneumonia

Interstitial pneumonia is most commonly produced by viral and mycoplasmal infections. In this type of pneumonia, the inflammatory process predominantly involves the walls and lining of the alveoli and the interstitial supporting structures of the lung, the alveoli septa.

Aspiration Pneumonia

The aspiration of esophageal or gastric contents into the lung can lead to the development of pneumonia. Aspiration of esophageal material can occur in patients with esophageal obstruction (e.g., tumor, stricture, and achalasia), diverticula (Zenker’s), or neuromuscular swallowing disturbances. Aspiration of liquid gastric contents is most often related to general anesthesia, tracheostomy, coma, or trauma.


Anthrax is caused by the sporelike microbe known as Bacillus anthracis. From the mid-1970s, there were no cases of anthrax in the United States until the biologic terrorist attacks using the bacillus that occurred in the fall of 2001. Anthrax is considered a highly volatile microbe because of its ease of transmission and high fatality rate. The organism can survive for decades in the soil in extreme conditions (heat and cold), without the need for a host.

There are three ways to contract anthrax: cutaneous, through an opening in the skin; inhalation (lungs), which is usually fatal (75%) if not treated in the early stages; and gastrointestinal. The cutaneous form is the most common type (75%) and is contracted by working with animals or animal byproducts (hides). Inhaled B. anthracis germinates in the lung tissue and lymph nodes, producing deadly toxins. These toxins cause cellular edema and disruption of normal cell function. Early signs are similar to those of influenza; however, progressive infection may cause labored breathing, shock, or even death. The gastrointestinal type, which causes intestinal inflammation, is usually caused by the consumption of contaminated meat.

Lung Abscess

A lung abscess is a necrotic area of pulmonary parenchyma containing purulent (puslike) material. A lung abscess may be a complication of bacterial pneumonia, bronchial obstruction, aspiration, a foreign body, or the hematogenous spread of organisms to the lungs either in a patient with diffuse bacteremia or as a result of septic emboli. Aspiration, which is the most common cause of lung abscesses, frequently occurs in the right lung because the right main bronchus is more vertical and larger in diameter than the left. The necrotic parenchyma becomes encapsulated by a fibrous wall, which encases the necrotic material. Unlike abscesses involving other organs, lung abscesses create an opening into the airway that can expand the extent of the infection.

Clinically a patient with a lung abscess has a fever and cough, and produces copious amounts of foul-smelling sputum. An important complication of lung abscess is the development of a brain abscess, which is produced by infected material carried by the blood from the lung to the left side of the heart and then on to the brain.

Radiographic Appearance

The earliest radiographic finding in lung abscess is a spherical density that characteristically has a dense center with a hazy, poorly defined periphery. If there is communication with the bronchial tree, the fluid contents of the cavity are partly replaced by air, producing a typical air-fluid level within the abscess (Figure 3-21). A cavitary lung abscess usually has a thickened wall with a shaggy, irregular inner margin. CT can assist in the diagnostic process to demonstrate an ill-defined outer wall and rule out empyema (Figure 3-22).


Tuberculosis is caused by Mycobacterium tuberculosis, a rod-shaped bacterium with a protective waxy coat that permits it to live outside the body for a long time. Tuberculosis spreads mainly by droplets in the air, which are produced in huge numbers by the coughing of an infected patient. Therefore, it is essential that respiratory precautions be followed by radiographers imaging patients with active disease to prevent spreading of the infection. The organisms may be inhaled from sputum that has dried and turned into dust. They are rapidly killed by direct sunlight but may survive a long time in the dark. Tuberculosis may also be acquired by drinking the milk of infected cows. However, routine pasteurization of milk has virtually eliminated this route of infection.

Unlike most bacteria, mycobacteria do not stain reliably by Gram method. However, once mycobacteria take up the stain, it is difficult to decolorize mycobacteria by either acid or alcohol, and thus the organisms are often called acid-fast bacilli.

Tuberculosis is primarily a disease of the lungs, although it can spread to involve the gastrointestinal, genitourinary, and skeletal systems. In the initial tuberculous infection (the primary lesion), a collection of inflammatory cells collects around a clump of tuberculosis bacilli to form a small mass (tubercle) that is visible to the naked eye. The outcome of this initial infection depends on the number of bacilli and the resistance of the infected tissue. If the resistance is good and the dose is small, the proliferation of fibrous tissue around the tumor limits the spread of infection and produces a mass of scar tissue. In the lung, tuberculous scars are commonly found in the posterior apical segments. They often contain calcium, which is deposited as healing occurs.

A larger dose of bacilli or lower patient resistance tends to permit the disease to progress slowly. Within the center of the tubercle, the bacilli kill inflammatory cells, so that the core becomes a necrotic, Swiss cheese–like mass (caseation). The caseous material may eventually become liquefied to form a cavity. Coalescence of several small cavities can result in the formation of a large cavity, which may contain an air-fluid level. Rupture of blood vessels crossing a cavity causes bleeding and the coughing up of blood (hemoptysis). An overwhelming infection with low resistance causes diffuse destruction throughout the lung, with the formation of huge cavities and often a fatal outcome.

The tuberculin skin test can detect previous tuberculous infection. The purified protein derivative (PPD) of the tuberculosis bacillus is injected into the skin, and the injection site examined 2 to 3 days later. A visible and palpable swelling 10 mm in diameter or larger indicates that the individual has developed antibodies to a previous exposure to the bacilli. If there is no such reaction, the individual has either not been exposed to the tuberculosis bacilli or is anergic (i.e., immunologically nonreacting). The tuberculin test is not positive during an acute infection or for several weeks thereafter. When dealing with a possibly infected patient, one must consider the 3- to 6-week incubation period and the fact that the tuberculin skin test does not become positive until 2 to 10 weeks after infection.

Primary Tuberculosis

Primary pulmonary tuberculosis has traditionally been considered a disease of children and young adults. However, with the dramatic decrease in the prevalence of tuberculosis (especially in children and young adults), primary pulmonary disease can develop at any age. The current decline is the result of wider screening and prevention programs.

Radiographic Appearance: There are four basic radiographic patterns of primary pulmonary tuberculosis, as follows:

Apr 10, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Respiratory System
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