Asthma Is a very common disease in which widespread narrowing of the airways develops because of an increased responsiveness of the tracheobronchial tree to various stimuli (allergens). Common allergens include house dust, pollen, molds, animal dander, certain fabrics, and various foods (extrinsic asthma). Exercise, heat or cold exposure, and emotional upset can also cause an asthma attack (intrinsic asthma). The hypersensitivity reaction to one or more of these allergens leads to swelling of the mucous membranes of the bronchi, excess secretion of mucus, and spasm of the smooth muscle in the bronchial walls, all of which lead to severe narrowing of the airways. This makes breathing (especially expiration) difficult and results in the characteristic wheezing sound that is produced by air passing through the narrowed bronchial tubes. Untreated or uncontrolled asthma permanently scars the bronchial structure, causing progressive disease.
Early in the course of the disease, chest radiographs obtained between acute episodes demonstrate no abnormalities. During an acute asthmatic attack, bronchial narrowing and difficulty in expiration lead to an increased volume of the hyperlucent lungs with flattening of the hemidiaphragms and an increase in the retrosternal air space. In asthma, unlike in emphysema, the pulmonary vascular markings remain normal. In patients with chronic asthma, especially those with a history of repeated episodes of superinfection, thickening of bronchial walls can produce prominence of interstitial markings and the “dirty chest” appearance. The results of the chest radiograph taken in the emergency room determine if the asthma has progressed to pneumonia.
Those patients with allergy-induced asthma can use preventive and rescue bronchodilators. Allergy shots may build up natural antibodies. Keeping airways open helps prevent infections, which asthmatics are prone to contract. New inhaled steroid drugs help control the inflammatory process and decrease the potential for developing pulmonary infection.
Bronchiectasis Refers to permanent abnormal dilation of one or more large bronchi as a result of destruction of the elastic and muscular components of the bronchial wall. Bronchitis, a destructive process, is a common complication of bronchiectasis and is nearly always the result of a bacterial infection. The infection may be either a severe necrotizing pneumonia or a result of a local or systemic abnormality that impairs the body’s defense mechanisms and promotes bacterial growth. Since the advent of antibiotic therapy and vaccines, the incidence of bronchiectasis has substantially decreased.
The patient with bronchiectasis typically has a chronic productive cough, often associated with recurrent episodes of acute pneumonia and hemoptysis. The disease usually involves the basal segments of the lower lobes, and it is bilateral in about half of the cases. Pulmonary function tests assist in the diagnostic process by determining any evidence of decreased gas exchange.
Plain chest radiographs may show coarseness and loss of definition of interstitial markings caused by peribronchial fibrosis and retained secretions. In more advanced disease, oval or circular cystic spaces can develop. These cystic dilatations can be up to 2 cm in diameter and often contain air-fluid levels. In very severe cases, coarse interstitial fibrosis surrounding local areas of dilatation can produce a honeycomb pattern.
Vaccines prevent many of the bacterial and viral infections that led to bronchiectasis in the past. Treatment of bronchiectasis consists of therapy to decrease the symptoms and an antibiotic based on the specific bacterial cause.
Carcinoma of lungs Primary carcinoma of the lung arises from the mucosa of the bronchial tree. The most common primary malignant lung neoplasm is bronchogenic carcinoma. Although its precise cause remains unknown, bronchogenic carcinoma has been closely linked to smoking and to the inhalation of cancer-causing agents (carcinogens), such as air pollution, exhaust gases, and industrial fumes. A major form of bronchogenic carcinoma is the solitary pulmonary nodule within the lung parenchyma.
The most common type of lung cancer is squamous carcinoma, which typically arises in the major central bronchi and causes gradual narrowing of the bronchial lumen. Adenocarcinomas usually arise in the periphery of the lung rather than in the larger central bronchi. The least common type of lung tumor is bronchiolar (alveolar cell) carcinoma. These 3 types are classified as non–small cell lung cancers and make up 80% of all lung cancers.
Although bronchogenic carcinoma may be diagnosed by detection of cancer cells in the sputum, a precise diagnosis usually requires biopsy of the tumor during bronchoscopy under CT or fluoroscopic guidance.
Bronchogenic carcinoma produces a broad spectrum of radiographic abnormalities that depend on the site of the tumor and its relationship to the bronchial tree. The tumor may appear as a discrete mass, or it may be undetectable and identified only by virtue of secondary changes resulting from an obstruction caused by the tumor within or compressing the bronchus.
Airway obstruction by bronchogenic carcinoma may cause atelectasis of a segment of lung and often leads to pneumonia that develops in the lung distal to the obstructed bronchus. An important radiographic sign differentiating this postobstructive pneumonia from simple inflammatory disease is the absence of an air bronchogram in the former. The air bronchogram can be detected only if there is an open airway leading to the area of consolidation.
Unilateral enlargement of the hilum, best appreciated on serial chest radiographs, may be the earliest sign of bronchogenic carcinoma. The enlarged hilum represents either a primary carcinoma arising in the major hilar bronchus or metastases to enlarged pulmonary lymph nodes from a small primary lesion elsewhere in the lung. CT is far superior to plain radiographs in detecting hilar and mediastinal lymphadenopathy and bronchial narrowing resulting from bronchogenic carcinoma.
Cavitation commonly occurs in bronchogenic carcinoma. It most often involves upper lung lesions and represents central necrosis of the neoplasm. The cavities usually resemble acute lung abscesses and have thick walls with irregular, often nodular, inner surfaces.
The prognosis for bronchogenic carcinoma is poor, except when the tumor is in the form of a solitary pulmonary nodule that can be surgically removed. Direct lymphatic spread of a tumor can cause enlargement of hilar or mediastinal lymph nodes. Distant metastases most frequently involve the bones, where they cause osteolytic destruction. Metastases to the liver, brain, and adrenal glands commonly develop.
Cystic fibrosis Is a generalized disorder resulting from a genetic defect transmitted as an autosomal recessive gene that affects the function of exocrine glands. It involves many organs in addition to the respiratory system, and nearly all exocrine glands are affected in varying distribution and degree of severity. These glands and other organs affected include the salivary glands, small bowel, pancreas, biliary tract, female cervix, and male genital system. In the respiratory system, evidence suggests that the lungs are histologically normal at birth. Pulmonary damage is initiated by gradually increasing secretions from hypertrophy of bronchial glands, leading to obstruction of the bronchial system. The resultant plugging promotes staphylococcal infection, followed by more tissue damage, as well as atelectasis (collapse of lung tissue) and emphysema. Once the cycle is in motion, it is difficult to stop. The signs and symptoms of cystic fibrosis usually include a chronic cough and wheezing associated with recurrent or chronic pulmonary infections. The cough is often accompanied by sputum, gagging, vomiting, and disturbed sleep. A barrel-chest deformity, clubbing of the fingers, and cyanosis occur as the disease progresses. In adolescents and adults the pulmonary complications associated with cystic fibrosis include pneumothorax, hemoptysis, and right-sided heart failure secondary to pulmonary hypertension.
The disease remains the most common lethal genetic disease for white children despite increasing life spans to the age of 20 years or older because of improved treatments. Its diagnosis rests largely on certain clinical and laboratory findings, most notably elevated sodium and chloride levels in sweat. Chest radiographs taken over a period of years aid in the diagnosis of cystic fibrosis by demonstrating gradually worsening structural abnormalities. Early changes of bronchial thickening and hyperinflation progress to extensive bronchiectasis, cyst formation, lobar atelectasis, scarring, pulmonary artery and right ventricular enlargement, and overinflation of the lung and chest wall. The development of a pneumothorax can be treated by closed chest tube thoracostomy drainage, and massive or recurrent hemoptysis is treated by embolizing involved bronchial arteries.
The prognosis associated with cystic fibrosis is determined by the degree of pulmonary involvement and varies greatly. However, respiratory failure resulting from deterioration of the lungs is inevitable and eventually leads to death in the late 20s to early 30s. Treatment methods include antimicrobial drugs to combat infection, bronchodilators administered through inhalers, and respiratory physical therapy.
Epiglottitis/Croup Epiglottitis – acute infections of the epiglottis, most commonly caused by Haemophilus influenzae in children, cause thickening of epiglottic tissue and the surrounding pharyngeal structures.
On lateral projections of the neck using soft tissue techniques, a rounded thickening of the epiglottic shadow gives it the configuration and approximate size of an adult’s thumb, in contrast to the normal, narrow epiglottic shadow resembling an adult’s little finger.
Prompt recognition of acute epiglottitis is imperative because the condition may result in sudden complete airway obstruction. Because of its severity, epiglottitis requires hospitalization so the patient may be monitored. Intubation may become necessary to restore normal respiration. Also, antibiotics may have to be administered to treat the infection, and corticosteroids to reduce the swelling.
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.
Frontal radiographs of the lower neck show a characteristic smooth, fusiform, tapered narrowing (hour-glass shape) of the subglottic airway caused by the edema.
A cool mist helps alleviate the breathing difficulty in patients with croup. At home, many patients use the steam from a hot shower for 15- to 20-minute intervals. When breathing continues to be difficult, medical attention should be sought. Corticosteroid treatment is used in severe cases to help reduce swelling.
Hyaline membrane disease Also known as respiratory distress syndrome (RDS). It is idiopathic, affects premature infants and is one of the most common causes of respiratory distress in the newborn 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 (where gas exchanges occur in the lungs). Normally the alveolar cell walls produce lipoprotein, which maintains the surface tension within the alveoli. This permits the alveoli to remain inflated so that atelectasis does not occur. This disease process results from surfactant deficiency resulting from cell immaturity or birth trauma.
The signs of RDS include rapid and labored breathing immediately or within a few hours after delivery with the atelectasis and respiratory failure progressively worsening. In severe cases respiratory and metabolic acidosis develop because blood passing through the lungs is not adequately oxygenated and its carbon dioxide is inadequately eliminated.
Chest radiographs demonstrate severe atelectasis with an air-bronchogram sign, characterized by bronchi surrounded by nonaerated alveoli (pronounced underaeration is seen). The radiographic hallmark of hyaline membrane disease is a finely granular appearance of the pulmonary parenchyma.
This is a life-threatening condition, but, if the infant’s ventilation is adequately supported, surfactant production should begin within a few days. Treatment consists of maintenance of a proper thermal environment and satisfactory levels of tissue oxygenation, which is monitored frequently via arterial blood gas measurements. In some instances, pulmonary surfactant may be introduced intratracheally to reduce the severity of the disease. Once the surfactant is present, RDS will resolve by 4 or 5 days.
New treatment advances include the use of an artificial surfactant which 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.
Methicillin resistant Staphylococcus Aureus (MRSA) MRSA infection is caused by Staphylococcus aureus bacteria — often called “staph.” It is a strain of staph that’s resistant to the broad-spectrum antibiotics commonly used to treat it. It is a nosocomial infection and multi-drug resistant. This means it is resistant to more than one antibiotic. Methicillin-resistant Staphylococcus aureus (MRSA) contribute to surgical wound, urinary tract, and bloodstream infections. MRSA can also cause respiratory infections. MRSA can be fatal.
Most MRSA infections occur in hospitals or other health care settings, such as nursing homes and dialysis centers. MRSA remains a concern in hospitals, where it can attack those most vulnerable — older adults and people with weakened immune systems, burns, surgical wounds or serious underlying health problems. This is particularly true if you have a hospital stay of more than 14 days. MRSA is also prevalent in long term care facilities. Carriers of MRSA have the ability to spread it, even if they’re not sick themselves.
Staph bacteria are normally found on the skin or in the nose of about one-third of the population. If you have staph on your skin or in your nose but aren’t sick, you are said to be “colonized” but not infected. Healthy people can be colonized and have no ill effects. However, they can pass the germ to others. Staph skin infections, including MRSA, generally start as small red bumps that resemble pimples, boils or spider bites. These can quickly turn into deep, painful abscesses that require surgical draining. Sometimes the bacteria remain confined to the skin. But they can also penetrate into the body, causing potentially life-threatening infections in bones, joints, surgical wounds, the bloodstream, heart valves and lungs.
Signs and symptoms of a wound infection include: redness, warmth and tenderness of the wound; the wound may contain pus; and the patient will have a fever.
Doctors diagnose MRSA by checking a tissue sample or nasal secretions for signs of drug-resistant bacteria. In the hospital, a patient may be tested for MRSA if they show signs of infection or if they are transferred into a hospital from another health care setting where MRSA is known to be present. A patient may also be tested if you have had a previous history of MRSA.
MRSA still respond to certain medications. In hospitals and care facilities, doctors often rely on the antibiotic vancomycin to treat resistant germs. Although vancomycin saves lives, it may become less effective as well. Some drugs that treat ordinary staph aren’t effective against MRSA, and their use could lead to serious illness and more resistant bacteria. In some cases, antibiotics may not be necessary. For example, doctors may drain a superficial abscess caused by MRSA rather than treat the infection with drugs.
Pneumoconiosis Prolonged occupational exposure to certain irritating particulates can cause severe pulmonary disease and a spectrum of radiographic findings. Inhaled foreign substances retained permanently in the acini cause irreversible damage. These inhaled particles cause a chronic interstitial inflammation that leads to pulmonary fibrosis and a diffuse nonspecific radiographic pattern of linear streaks and nodules throughout the lungs. The inflammation initially causes injury to the mucosal lining; long-term exposure may injure the pulmonary parenchyma and even lead to the development of a malignant neoplasm. The severity of the pneumoconiosis depends on the size of the particles, the length of exposure, and the concentration of particulates in the atmosphere (type of exposure). The more severe the exposure, the more fibrotic the lung becomes and the greater the resultant shortness of breath. The most common of the pneumoconioses are silicosis, asbestosis, and anthracosis (coal worker’s disease). Other causes include exposure to such dusts as tin, iron oxide, barium, and beryllium. As many as 40 minerals cause lung lesions when inhaled, although most do not produce morphologic or functional abnormalities.
Initially, multiple small, irregular opacities produce a reticular pattern similar to that of silicosis. The nodules are not well defined and they tend to have a granular density. With advanced disease, the pattern of progressive massive fibrosis can develop. In progressive massive fibrosis, one or more masses of fibrous tissue with smooth, well-defined lateral borders gradually migrate toward the hilum, leaving a zone of hyperinflated emphysematous lung between the fibrous mass and the chest wall. A single large homogeneous mass in the perihilar area of one lung may simulate bronchogenic carcinoma; an occupational history is necessary to make the proper diagnosis of pneumoconiosis.
Today, there is no effective treatment for pneumoconiosis. Once the particles have embedded in the pulmonary tissue, the lungs deteriorate and lose the ability to remove them. The best available treatment is simply to avoid further exposure. Treatment is limited to addressing complications of the disease. Patients with advanced disease that has become malignant may require lung resection to remove the cancerous tissue, radiation therapy to shrink the tumor, or chemotherapy.
Pneumonia 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, or air-space 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. 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).
Consolidation of the lung parenchyma with little or no involvement of the airways produces the characteristic air-bronchogram sign. 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. 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 (e.g. 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.
The small patches of consolidation may be seen radiographically as opacifications that are scattered throughout the lungs, but are separated by an abundance of air-containing lung tissue; air bronchograms are absent. If consolidation causes obstructed airways, atelectasis is evident.
Interstitial pneumonia is most commonly produced by viral and mycoplasmal infections. In this type of pneumonia, the inflammatory process involves predominantly the walls and lining of the alveoli and the interstitial supporting structures of the lung, the alveoli septa.
The interstitial dispersal of the infection produces a linear or reticular pattern. When seen on end, the thickened interstitium may appear as multiple small nodular densities. Left untreated, interstitial pneumonia may cause “honeycomb lung,” which is demonstrated by CT as cystlike spaces and dense fibrotic walls.
Extensive inflammation of the lung can cause a mixed pattern of alveolar, bronchial, and interstitial pneumonias, and this pattern appears as opacifications representing pulmonary consolidation. Treatment for these types of pneumonias usually includes regimented doses of an antibiotic to eradicate the cause. Rest, hydration, and deep-breathing techniques (supportive therapy) help in treating the infectious process.
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 anesthetic, tracheostomy, coma, or trauma.
Both types of aspiration cause multiple alveolar densities, which may be distributed widely and diffusely throughout both lungs. Because the anatomic distribution of pulmonary changes is affected by gravity, the posterior segments of the upper and lower lobes are most commonly affected, especially in debilitated or bedridden patients.
For effective treatment, early diagnosis of aspiration pneumonia and the prompt administration of corticosteroid and antibiotic therapy are essential to improve the otherwise grave prognosis.
Pulmonary edema Refers to an abnormal accumulation of fluid in the extravascular pulmonary tissues. The most common cause of pulmonary edema is an elevation of the pulmonary venous pressure. This is most often attributed to left-sided heart failure, but may also be caused by pulmonary venous obstruction (mitral valve disease, left atrial tumor) or lymphatic blockade (fibrotic, inflammatory, or metastatic disease involving the mediastinal lymph nodes). Other causes of pulmonary edema include uremia, narcotic overdose, exposure to noxious fumes, excessive oxygen, high altitudes, fat embolism, adult respiratory distress syndrome, and various neurologic abnormalities.
Transudation of fluid into the interstitial spaces of the lungs is the earliest stage of pulmonary edema. However, in patients with CHF or pulmonary venous hypertension, increased pulmonary venous pressure first appears as a redistribution of blood flow from the lower to the upper lung zones. Redistribution causes prominent enlargement of the superior pulmonary veins and decreased caliber of the veins draining the inferior portions of the lung. Edema fluid in the interstitial space causes a loss of the normal sharp definition of pulmonary vascular markings. Accentuation of the vascular markings about the hila produces a perihilar haze. Fluid in the interlobular septa produces characteristic thin horizontal lines of increased density at the axillary margins of the lung inferiorly.
A further increase in pulmonary venous pressure leads to the development of alveolar or pleural transudates. Alveolar edema appears as irregular, poorly defined patchy densities scattered throughout the lungs. The classic radiographic finding of alveolar pulmonary edema is the butterfly (or bat’s-wing) pattern, a diffuse, bilaterally symmetric, fan-shaped infiltration that is most prominent in the central portion of the lungs and fades toward the periphery.
Pleural effusion associated with pulmonary edema usually occurs on the right side. When bilateral, the effusion tends to be more noticeable on the right. There is often an associated thickening of the interlobar fissures. Pleural effusions are best demonstrated radiographically using a horizontal beam with the patient in a lateral decubitus position.
After adequate treatment of pulmonary edema, the interstitial, alveolar, and pleural abnormalities may disappear within several hours. Loculated pleural fluid within a fissure (especially the minor fissure) may resorb more slowly and appear as a sharply defined, elliptical, or circular density that simulates a solid parenchymal mass.
Most patients with pulmonary edema caused by CHF or other heart disease have evidence of cardiomegaly. When the cause of the pulmonary edema is noncardiogenic, the heart often remains normal in size.
The nonpharmacologic approach includes avoiding excessive physical stress, decreasing dietary salt, and wearing compressive stockings to decrease the incidence of deep vein thrombosis (DVT). Pharmacologic therapy includes some combination of the following drugs: diuretics, angiotensin-converting enzyme inhibitors, digoxin (digitalis), parenteral inotropic agents, calcium channel blockers, beta blockers, and antithrombotic therapy.
Pulmonary infarct An infarct is a localized area of ischemic necrosis within a tissue or organ produced by occlusion of either its arterial supply or its venous drainage. The two most common clinical forms of infarction are myocardial and pulmonary. Almost all infarcts result from thrombotic or embolic occlusion. When a patient has a pulmonary embolism, sometimes the blockage of blood flow causes lung tissue to die causing pulmonary infarction.
In spite of the dual blood supply from bronchial and pulmonary vessels, pulmonary infarction is very common. Infarction is common when the circulation of the lung is slowed down with associated increased pulmonary circulatory pressure (e.g. post-operative or post-natal). Under such conditions, when a branch of the pulmonary artery is blocked, force of the bronchial arteries is insufficient to supply the obstructed area due to increased pulmonary circulatory pressure. Blood drains into the area from all the connections and stagnates there. Vessels in the alveolar walls give way and blood escapes into the alveolar space and the whole area becomes dead and coagulated into a firm blood-filled solid, airless mass.
Causes of infarction are emboli (DVT) that travel through the blood stream to the lungs to block the pulmonary artery; pulmonary thrombosis due to atherosclerosis of the pulmonary artery.
Radiographically, a pulmonary opacity develops distal to the occluded pulmonary artery. “Hampton’s hump” is a radiologic sign seen on chest radiographs indicating pulmonary infarction and atelectasis due to pulmonary embolism. It consists of a pleura based shallow wedge-shaped consolidation in the lung periphery with the base against the pleural surface and its apex towards the hilum.
Scleroderma Means “hard skin”. There are many human diseases associated with tightening and thickening of the skin so there are many “sclerodermas”.
Systemic sclerosis is the most serious form of the disease. This form of scleroderma can occur at any age but is most common in women of childbearing age. It is the most fatal of all the rheumatologic diseases.
Systemic scleroderma is very unpredictable although most cases can be classified into one of four different general patterns of disease. The illness is classified based on the extent and severity of skin thickening which in turn is related to the risk profile of developing internal organ involvement. Disability and survival are mainly influenced by the presence of damage to the lungs, kidneys, heart and gastrointestinal systems.
The cause of scleroderma is not currently understood and there are no proven effective therapies for the underlying disease process.
The lungs are involved in around 80% of all patients with scleroderma. Lung involvement in all its forms has emerged to be the leading cause of death and disability. Lung involvement occurs in both diffuse and limited scleroderma; thus all patients need to be concerned about this potential complication.
Involvement of the lung causes shortness of breath or fatigue during physical activity. Many patients with scleroderma become less physically active because of musculoskeletal complaints or the fatiguing nature of the illness. Other patients develop a dry, non-productive cough which also might worsen with physical activity.
Several different processes that are typical of the scleroderma disease process may be present and in different levels of contribution. The key elements of scleroderma lung disease involve 1) inflammation (potentially treatable); 2) lung scarring (not reversible but potentially preventable); and 3) blood vessel injury (treatable)
Inflammation and scarring of the lung tissue is called interstitial lung disease or ILD. ILD may be suspected if the bases of the lungs make crackling sounds on stethoscope examination. ILD is best assessed by complete pulmonary function testing. Lung volume will be reduced if the lungs are stiffened by scar.
The most commonly used test to determine how much inflammation is present versus how much scar is a high resolution CT scan of the lungs. CT can detect scarring that would be missed by simple chest X-ray and can help to assess the presence and distribution of lung inflammation.
Some patients in selected situations need to take the more definitive step of lung biopsy
Sinusitis The paranasal sinuses (maxillary, ethmoid, frontal, and sphenoid) are paired, air-filled cavities that are lined with a mucous membrane that is directly continuous with the nasal mucosa. The size and shape of the sinuses vary in different age periods, in different individuals, and on the two sides of the same individual. At birth, the maxillary sinus is only a slitlike space that later expands to fill the maxilla and is thus responsible for the growth of the face. The ethmoid sinuses can be seen radiographically by 6 years of age, whereas the frontal sinuses usually are not well demonstrated until about 10 years of age. The sphenoid sinuses begin to develop around 2 or 3 years of age and are fully developed by late adolescence.
Viral infection of the upper respiratory tract may lead to obstruction of drainage of the paranasal sinuses and the development of localized pain, tenderness, and fever.
Radiographically, acute or chronic sinusitis causes mucosal thickening, which appears as a soft tissue density lining the walls of the involved sinuses. The maxillary antra are most commonly affected and are best visualized on the Waters’ projection. An air-fluid level in a sinus is usually considered a manifestation of acute inflammatory disease. To demonstrate this finding, it is essential that all sinus films be obtained with the patient erect and with the use of a horizontal beam. The destruction of the bony wall of a sinus is an ominous sign indicating secondary osteomyelitis. CT, the procedure of choice, demonstrates bony sinonasal anatomy; coronal images can show air-fluid levels. Coronal MRI provides the best method to detect suspected complications, such as mucocele, osteomyelitis, or underlying intracranial disease.
Sinusitis caused by bacteria is treated with antibiotics to eradicate the infection. Decongestants may be taken to relieve symptoms and aid in sinus drainage. Steroid nasal sprays help reduce mucosal inflammation. Chronic sinusitis may require surgery to clean and drain the sinus, and to repair a deviated septum or nasal obstruction that may be the cause of recurrent inflammation.
Tuberculosis Is caused by Mycobacterium tuberculosis, a rod-shaped bacterium (acid-fast bacilli) that lives outside the body for a long time. Tuberculosis spreads mainly by droplets in the air (produced by coughing). Respiratory precautions must be followed when radiographing patients with active disease. 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 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. This material may eventually become liquefied to form a cavity. The fusion 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 non-reacting). The tuberculin test is not positive during an acute infection or for several weeks thereafter.