2 L/min oxygen nasal cannula were pH 7.51, PaCO2 29 mm Hg, 
23 mEq/L, PaO2 66 mm Hg, and SaO2 94%. On the basis of these clinical data, the following SOAP was documented.
Respiratory Assessment and Plan
S “I've coughed up a cup of sputum since breakfast.”
O Vital signs: BP 155/85, HR 90, RR 22, T normal; perspiring and weak and cyanotic appearance; voice hoarse-sounding; weak cough; large amounts of blood-streaked sputum; dull percussion notes over left lower lobe; wheezing and coarse crackles throughout both lung fields; recent PFTs: restrictive and obstructive pulmonary disorder; CT scan and CXR: 2- to 5- cm masses in right and left mediastinum in hilar regions and atelectasis of left lower lobe. Bronchoscopy: Protruding tumors in both left and right large airways, mucus plugging. Biopsy: Squamous cell bronchogenic carcinoma. ABGs (2 L/min O2 by nasal cannula): pH 7.51, PaCO2
29, 
23, PaO2 66, SaO2 94%. A
•Bronchogenic carcinoma (CT scan and biopsy)
•Respiratory distress (vital signs, ABGs)
•Bronchospasm (wheezing)
•Excessive bloody bronchial secretions (sputum, coarse crackles)
•Mucus plugging (bronchoscopy)
•Poor ability to mobilize secretions (weak cough)
•Atelectasis of left lower lobe (CXR)
•Acute alveolar hyperventilation with mild hypoxemia (ABGs)
P Up-regulate Oxygen Therapy Protocol (4 L nasal cannula and titration by oximetry). Also begin Aerosolized Medication Protocol (0.5 mL albuterol in 2 mL NS q6h), followed by Airway Clearance Therapy Protocol (DB&C). Begin Lung Expansion Therapy Protocol (incentive spirometry q2 h and prn). Closely monitor and reevaluate.
Three Days After Admission
A respiratory therapist evaluated the patient during morning rounds. After reviewing the patient's chart, the practitioner went to the patient's bedside and discovered that the man was not tolerating the chemotherapy well. He had been vomiting intermittently for the past 10 hours and was still in obvious respiratory distress. He appeared cyanotic and tired, and his hospital gown was wet from perspiration. His cough was still weak and productive of large amounts of moderately thick, clear, and white sputum. He stated in a hoarse voice that he was still not breathing very well.
His vital signs were blood pressure 166/90 mm Hg, heart rate 95 beats/min, respiratory rate 28 breaths/min, and temperature normal. Dull percussion notes were elicited over both the right and left lower lobes. Wheezing and coarse crackles were auscultated throughout both lung fields. His ABG values on a 4.0 L/min cannula were pH 7.55, PaCO2
25 mm Hg, 
21 mEq/L/min, PaO2 53 mm Hg, and SaO2 92%.
On the basis of these clinical data, the following SOAP was documented.
Respiratory Assessment and Plan
S “I'm still not breathing very well.”
O Vital signs: BP 166/90, HR 95, RR 28, T normal; vomiting over past 10 hours; cyanosis, tiredness, and dampness from perspiration; cough: weak and productive of moderately thick, clear, and white sputum; dull percussion notes over both right and left lower lobes; wheezing and coarse crackles over both lung fields; ABGs on a 4 L/min cannula pH 7.55, PaCO2 25,
21, PaO2 53, SaO2 92%.
A
•Bronchogenic carcinoma (previous CT scan and biopsy)
•Not tolerating chemotherapy well (excessive vomiting)
•Continued respiratory distress
•Bronchospasm (wheezing)
•Excessive bronchial secretions (sputum, coarse crackles)
•Mucus plugging still likely (previous bronchoscopy, secretions becoming thicker)
•Poor ability to mobilize secretions (weak cough)
•Atelectasis of left lower lobes; atelectasis likely in right lower lobe now (CXR, dull percussion notes)
•Acute alveolar hyperventilation with moderate hypoxemia, worsening (ABGs)
•Possible impending ventilatory failure (ABGs, weak cough, worsening vital signs) P Up-regulate Oxygen Therapy Protocol (simple oxygen mask). Up-regulate Aerosolized Medication Protocol (increasing treatment frequency to q3h; consider adding acetylcysteine q6h). Up-regulate Airway Clearance Therapy Protocol (CPT and PD q3h). Up-regulate Lung Expansion Therapy Protocol (change incentive spirometry to +5 to +10 cm H2O CPAP mask,
qid). Contact physician about possible ventilatory failure. Discuss therapeutic bronchoscopy. Closely monitor and reevaluate.
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Sixteen Days After Admission
Although the physician's original intention and hope were to discharge the patient soon, stabilizing the man for any length of time proved difficult. Over the next 2 weeks, the patient had continued to be nauseated on a daily basis. He did, however, have occasional periods of relief during which he could breathe easier, but he generally was in respiratory distress. On day 16 the respiratory therapist observed and collected the following clinical data.
The patient was lying in bed in the supine position. His eyes were closed, and he was unresponsive to the therapist's questions. The patient was in obvious respiratory distress. He appeared pale, cyanotic, and diaphoretic. No cough was observed at this time, but coarse crackles could easily be heard from across the patient's room. The nurse in the patient's room stated that the doctor had called the coarse crackles a “death rattle.” The patient's vital signs were blood pressure 170/105 mm Hg, heart rate 110 beats/min, respiratory rate 12 breaths/min and shallow, and rectal temperature normal. Percussion was not performed. Wheezing and coarse crackles were heard throughout both lung fields. On an FIO2 of 0.60,
his ABG values were pH 7.28, PaCO2 63 mm Hg, 
28 mEq/L, PaO2 66 mm Hg, and SaO2 89%. At that time, the following SOAP was recorded.
Respiratory Assessment and Plan
S N/A (patient comatose)
O Unresponsive; pale, cyanotic, and perspiring appearance; no cough noted; coarse crackles heard without stethoscope; vital signs BP 170/105, HR 110, RR 12 and shallow, T normal;
wheezing and coarse crackles over both lung fields; ABGs are pH 7.28, PaCO2 63, 
28, PaO2 66, SaO2 89%.
A
•Bronchogenic carcinoma (previous CT scan and biopsy)
•Bronchospasm (wheezing)
•Excessive bronchial secretions (coarse crackles)
•Mucus plugging still likely (previous bronchoscopy, coarse crackles)
•Poor ability to mobilize secretions (no cough)
•Atelectasis (CXR)
•Acute ventilatory failure with moderate hypoxemia (ABGs)—worsening
P Contact physician about acute ventilatory failure, and discuss code status; and the need to up-regulate Oxygen Therapy Protocol, Airway Clearance Therapy Protocol, and Aerosolized Medication Therapy Protocol. Monitor and reevaluate.
Discussion
This case demonstrates the few specific treatments that a respiratory therapist can bring to the care of patients with lung cancer. Specifically, it illustrates that most of the patients who have concomitant obstructive pulmonary disease have a need for a good Airway Clearance Therapy Protocol (Protocol 10.2). Comfort of the patient must be kept in mind at all times.
The first assessment was performed soon after bronchoscopy and diagnosis. The patient's blood-stained sputum could have reflected the primary tumor or, as likely, bleeding from the bronchoscopy sites. In such cases the practitioner must monitor this sputum as the days go along. No improvement in the patient's wheezing can be expected if a bronchial tumor is the cause, but it may improve if bronchospasm (from cigarette smoking) is the causative factor.
The wheezing and coarse crackles indicated the need for vigorous airway clearance therapy. The atelectasis in the left lower lobe suggested that a trial of careful Lung Expansion Therapy Protocol (Protocol 10.3) and Aerosolized Medication Therapy Protocol (Protocol 10.4) were in order. The ABG values assessed with the patient on 2 L/min oxygen showed acute alveolar hyperventilation with moderate hypoxemia. At this time, the patient's oxygen therapy was up-regulated to a 4 L/min nasal cannula. Certainly, a trial of oxygen therapy via an air-entrainment mask (or nonrebreathing mask) also would have been appropriate. Patient anxiety may be alleviated with appropriate treatment of the hypoxemia.
The second assessment revealed that the patient may have developed atelectasis in both the right and left lower lobes (where the tumor masses had been noted previously). This case may present a setting in which therapeutic bronchoscopy or laser-assisted endobronchial resection of the tumor masses may be helpful. The patient continued to be hypoxemic, despite alveolar hyperventilation. A higher FIO2 (e.g., through a Venturi oxygen mask) was indicated.
Vigorous suctioning was appropriate. Because of the impending ventilatory failure, ordering at least one cycle of ventilator support, perhaps in the form of noninvasive positive pressure ventilation (see Chapter 11, Respiratory Insufficiency, Respiratory Failure, and Ventilatory Management Protocols), for such a patient would not be surprising given that he had just recently received radiation and chemotherapy. The patient's wishes in this respect should have been checked against his Living Will or Durable Power of Attorney for Health Care (end-of-life directives), if such a document existed.
The last assessment indicates that the patient had slipped into acute ventilatory failure. All health care personnel had agreed that the patient was close to death. The practitioner may be excused for not suggesting the use of chest physical therapy and postural drainage at this time, because of the patient's wishes. Aerosolized morphine is now being used to relieve dyspnea in terminally ill cancer patients. If, however, aggressive therapy was still in order, formal evaluation and treatment of superimposed atelectasis or pneumonia, or both, would be in order.
Self-Assessment Questions
1.Which of the following is commonly located near a central bronchus or hilus and projects into the large bronchi?
a.Squamous cell carcinoma
b.Oat cell carcinoma
c.Large cell carcinoma
d.Adenocarcinoma
2.Which of the following arises from the mucous glands of the tracheobronchial tree?
a.Small cell carcinoma
b.Adenocarcinoma
c.Squamous cell carcinoma
d.Oat cell carcinoma
3.Which of the following carcinomas has the strongest correlation with cigarette smoking?
a.Adenocarcinoma
b.Small cell carcinoma
c.Large cell carcinoma
d.Squamous cell carcinoma
4.Which of the following has the fastest growth (doubling) rate?
a.Large cell carcinoma
b.Small cell carcinoma
c.Adenocarcinoma
d.Squamous cell carcinoma
5.Which of the following is(are) associated with bronchogenic carcinoma?
1.Alveolar consolidation
2.Pleural effusion
3.Alveolar hyperinflation
4.Atelectasis
a.2 and 3 only
b.1 and 4 only
c.2 and 3 only
d.1, 2, and 4 only
1The role of the respiratory therapist as a patient educator is becoming increasingly important and nowhere more so than in the field of smoking cessation education. This function occurs best in outpatient and inpatient settings as part of wellorganized pulmonary rehabilitation programs, in the public domain (e.g., lectures to high school students), and on an individual basis with patients. The role of smoking cessation education has been discussed elsewhere (see Chapter 13, Chronic Obstructive Pulmonary Disease, Chronic Bronchitis, and Emphysema) as part of evidence-based practice in chronic obstructive pulmonary disease (COPD). Documentation of efforts and patient adherence and compliance to smoking cessation efforts has become increasingly complex and important for reimbursement purposes. The effect of smoking cessation on established lung cancer is, unfortunately, not particularly successful.
2Pack-years = packs per day × years smoked; e.g., one pack of cigarettes smoked per day × 20 years = 20 pack-years. 3Modified from the American Cancer Society, http://www.cancer.org.
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PA R T I X
Environmental Lung Diseases
OUTLINE
Chapter 27 Interstitial Lung Diseases
C H A P T E R 2 7
Interstitial Lung Diseases
CHAPTER OUTLINE
Anatomic Alterations of the Lungs
Etiology and Epidemiology
Interstitial Lung Diseases of Known Causes or Associations
Systemic Diseases
Idiopathic Interstitial Pneumonias
Specific Pathology
Miscellaneous Diffuse Interstitial Lung Diseases
Overview of the Cardiopulmonary Clinical Manifestations Associated With Chronic Interstitial Lung Diseases
General Management of Interstitial Lung Disease
Medications and Procedures Commonly Prescribed by the Physician
Respiratory Care Treatment Protocols
Other Treatment
Case Study: Interstitial Lung Disease
Self-Assessment Questions
CHAPTER OBJECTIVES
After reading this chapter, you will be able to:
•List the anatomic alterations of the lungs associated with chronic interstitial lung disease.
•Describe the causes of chronic interstitial lung disease.
•List the cardiopulmonary clinical manifestations associated with chronic interstitial lung disease.
•Describe the general management of chronic interstitial lung disease.
•Describe the clinical strategies and rationales of the SOAPs presented in the case study.
•Define key terms and complete self-assessment questions at the end of the chapter and on Evolve
KEY TERMS
Allergic Alveolitis
Angiotensin Converting Enzyme (ACE Test)
Asbestos
Asbestosis
Beryllium
Berylliosis
Black Lung
Bronchial Lavage
Bronchiolitis Obliterans Organizing Pneumonia (BOOP)
Caplan Syndrome
Chronic Eosinophilic Pneumonia
Churg-Strauss Syndrome
Coal Miner Lung
Coal Worker Pneumoconiosis (CWP)
Connective Tissue (Collagen Vascular) Disorders
Cryptogenic Organizing Pneumonia (COP)
Desquamative Interstitial Pneumonia (DIP)
Extrinsic Allergic Alveolitis
Farmer Lung
Focal Emphysema
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Glomerular Basement Membrane Goodpasture Syndrome Hemoptysis
Honeycombing Hypersensitivity Pneumonitis
Idiopathic Pulmonary Fibrosis (IPF)
Idiopathic Pulmonary Hemosiderosis Interstitial Lung Disease (ILD)
Late Fibrotic Phase Lymphangioleiomyomatosis (LAM) Lymphocytic Interstitial Pneumonia (LIP) Lymphomatoid Granulomatosis Mononeuritus Multiplex
Plasmapheresis Pleural Calcifications Pneumoconiosis
Polymyositis-Dermatomyositis Progressive Massive Fibrosis (PMF) Progressive Systemic Sclerosis (PSS) Pulmonary Alveolar Proteinosis
Pulmonary Langerhans Cell Histiocytosis (PLCH) Pulmonary Vasculitides
Quartz Silicosis (Grinder Disease) Rheumatoid Pneumoconiosis Sarcoidosis
Scleroderma Silica Silicosis
Sjögren Syndrome
Systemic Lupus Erythematosus (SLE)
Usual Interstitial Pneumonia (UIP)
Wegener Granulomatosis
The term interstitial lung disease (ILD) (also called diffuse interstitial lung disease, fibrotic interstitial lung disease, and pulmonary fibrosis) refers to a broad group of inflammatory lung disorders. More than 180 disease entities are characterized by acute, subacute, or chronic inflammatory infiltration of alveolar walls by cells, fluid, and connective tissue. If left untreated, the inflammatory process can progress to irreversible pulmonary fibrosis. The ILD group consists of a wide range of illnesses with varied causes, treatments, and prognoses. However, because the ILDs all reflect similar anatomic alterations of the lungs and therefore cardiopulmonary clinical manifestations, they are presented as a group in this chapter.
Anatomic Alterations of the Lungs
The anatomic alterations of ILD may involve the bronchi, alveolar walls, and adjacent alveolar spaces. In severe cases the extensive inflammation leads to pulmonary fibrosis, granulomas, honeycombing, and cavitation. During the acute stage of any ILD, the general inflammatory condition is characterized by edema and the infiltration of a variety of white blood cells (e.g., neutrophils, eosinophils, basophils, monocytes, macrophages, and lymphocytes) in the alveolar walls and interstitial spaces (Fig. 27.1A). Bronchial inflammation and thickening and increasing airway secretions also may be present.
FIGURE 27.1 (A) Interstitial lung disease. Cross-sectional microscopic view of alveolar-capillary unit. B, Basophil; E, eosinophil; FIB, fibroblast (fibrosis); L, lymphocyte; M, monocyte; MAC, macrophage; N, neutrophil; PC, pulmonary capillary; RBC, red blood cell; TI, type I alveolar cell; TII, type II alveolar cell. (B) Asbestosis (close-up of one alveolar unit). AF, Asbestos fiber; FIB, fibrosis; M, macrophage.
During the chronic stage, the general inflammatory response is also characterized by the infiltration of large numbers of various white blood cells (especially monocytes, macrophages, and lymphocytes) and some fibroblasts may be present in the alveolar walls and interstitial spaces. This stage may be followed by further interstitial thickening, fibrosis, granulomas, and, in some cases, honeycombing and cavity formation. Pleural effusion may be present. In the chronic stages the basic pathologic features of interstitial fibrosis are identical in any interstitial lung disorder (so-called end-stage pulmonary fibrosis).
As a general rule the interstitial lung disorders produce restrictive lung conditions. However, because bronchial inflammation and excessive airway secretions can develop in the small airways, the clinical manifestations associated with an obstructive lung disorder also may be seen. Therefore the patient with ILD may demonstrate a restrictive disorder, an obstructive disorder, or a combination of both.
The major pathologic or structural changes associated with chronic ILDs are as follows:
•Destruction of the alveoli and adjacent pulmonary capillaries
•Fibrotic thickening of the respiratory bronchioles, alveolar ducts, and alveoli
•Granulomas
•Honeycombing and cavity formation
•Fibrocalcific pleural plaques (particularly in asbestosis)
•Bronchospasm
•Excessive bronchial secretions (caused by inflammation of airways)
Etiology and Epidemiology
Because there are more than 180 different pulmonary disorders classified as ILD, it is helpful to group them according to their occupational or environmental exposure, disease associations, and specific pathology. Table 27.1 provides an overview of common ILD groups. A discussion of the more common ILDs follows.
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TABLE 27.1
Overview of Interstitial Lung Diseases
|
Occupational, |
|
Idiopathic |
|
Miscellaneous |
|
Environmental, and |
Systemic Diseases |
Interstitial |
Specific Pathology |
|
ILDs |
|
Therapeutic Exposures |
|
Pneumonia |
|
|
|
|
|
|
Occupation/Environmental |
Connective Tissue |
|
|
|
|
|
Disease |
|
|
|
|
Inorganic Substance |
• Scleroderma |
• Idiopathic |
• |
• Goodpasture |
|
Exposure |
• Rheumatoid |
pulmonary |
Lymphangioleiomyomatosis |
syndrome |
|
• Asbestosis |
arthritis |
fibrosis |
(LAM) |
• Idiopathic |
|
• Coal dust |
• Sjögren |
• Nonspecific |
• Pulmonary Langerhans cell |
pulmonary |
|
• Silica |
syndrome |
cryptogenic |
histiocytosis |
hemosiderosis |
|
• Beryllium |
• Polymyositis or |
organizing |
• Pulmonary alveolar |
• Chronic |
|
• Aluminum |
dermatomyositis |
pneumonia |
proteinosis |
eosinophilic |
|
• Barium |
• Systemic lupus |
(BOOP) |
• The pulmonary |
pneumonia |
|
• Clay |
erythematosus |
• |
vasculitides |
|
|
• Iron |
|
Lymphocytic |
• Wegener granulomatosis |
|
|
Sarcoidosis |
|
|
• Certain talcs |
interstitial |
• Churg-Strauss syndrome |
|
|
|
|
|
Organic Exposure |
|
pneumonia |
• Lymphomatoid |
|
|
• Hypersensitivity |
|
(LIP) |
granulomatosis |
|
|
pneumonitis |
|
|
|
|
|
• Moldy hay |
|
|
|
|
|
• Silage |
|
|
|
|
|
• Moldy sugar cane |
|
|
|
|
|
• Mushroom compost |
|
|
|
|
|
• Barley |
|
|
|
|
|
• Cheese |
|
|
|
|
|
• Wood pulp, bark, dust |
|
|
|
|
|
• Cork dust |
|
|
|
|
|
• Bird droppings |
|
|
|
|
|
• Paints |
|
|
|
|
|
Medications and Illicit |
|
|
|
|
|
Drugs |
|
|
|
|
|
• Antibiotics |
|
|
|
|
|
• Antiinflammatory agents |
|
|
|
|
|
• Cardiovascular agents |
|
|
|
|
|
• Chemotherapeutic |
|
|
|
|
|
agents |
|
|
|
|
|
• Drug-induced systemic |
|
|
|
|
|
lupus erythematosus |
|
|
|
|
|
• Illicit drugs |
|
|
|
|
|
Radiation Therapy |
|
|
|
|
|
Irritant Gases |
|
|
|
|
Interstitial Lung Diseases of Known Causes or Associations (Pneumoconioses)
Occupational, Environmental, and Therapeutic Exposures
Inorganic Particulate (Dust) Exposure
Asbestos.
Exposure to asbestos may cause asbestosis, a common form of ILD. Asbestos fibers are a mixture of fibrous minerals composed of hydrous silicates of magnesium, sodium, and iron in various proportions. There are two primary types: the amphiboles (crocidolite, amosite, and anthophyllite) and chrysotile (most commonly used in industry). Asbestos fibers typically range from 50 to 100 µm in length and are about 0.5 µm in diameter. The chrysotiles have the longest and strongest fibers. Box 27.1 lists common sources associated with asbestos fibers.
Box 27.1
Common Sources Associated With Asbestos Fibers
•Acoustic products
•Automobile undercoating
•Brake lining
•Cements
•Clutch casings
•Floor tiles
•Fire-fighting suits
•Fireproof paints
•Insulation
•Roofing materials
•Ropes
•Steam pipe material
As shown in Fig. 27.1B, asbestos fibers can be seen by microscope within the thickened septa as brown or orange batonlike structures. The fibers characteristically stain for iron with Perls stain. The pathologic process may affect only one lung, a lobe, or a segment of a lobe, although multilobe involvement is the most common. The lower lobes are most
commonly affected. Pleural calcification is common and diagnostic in patients with an asbestos exposure history (see Fig. 27.5).
Coal Dust.
The pulmonary deposition and accumulation of large amounts of coal dust cause coal worker pneumoconiosis (CWP) (Fig. 27.2). CWP is also known as coal miner lung and black lung. Miners who use cutting machines at the coalface have the greatest exposure, but even relatively minor exposures may result in the disease. Indeed, cases have been reported in which coal miners’ wives developed the disease, presumably from shaking the dust from their husbands’ work clothes.
FIGURE 27.2 Coal worker pneumoconiosis, microscopic view. With massive amounts of inhaled particles (as in black lung disease in coal miners), a fibrogenic response can be elicited to produce the coal worker's pneumoconiosis with the coal macule seen here. Progressive massive fibrosis results. (From Klatt, E. [2010]. Robbins and Cotran atlas of pathology [2nd ed.]. Philadelphia, PA:
Elsevier.)
Simple CWP is characterized by the presence of pinpoint nodules called coal macules (black spots) throughout the lungs. The coal macules often develop around the firstand second-generation respiratory bronchioles and cause the adjacent alveoli to retract. This condition is called focal emphysema.
Complicated CWP or progressive massive fibrosis (PMF) is characterized by areas of fibrotic nodules greater than 1 cm in diameter. The fibrotic nodules generally appear in the peripheral regions of upper lobes and extend toward the hilum with growth. The nodules are composed of dense collagenous tissue with black pigmentation. Coal dust by itself is chemically inert. The fibrotic changes in CWP are usually caused by silica.
Silica.
Silicosis (also called quartz silicosis or grinder disease) is caused by the chronic inhalation of crystalline, free silica, or silicon dioxide particles. Silica is the main component of more than 95% of the rocks of the earth. It is found in sandstone, quartz (beach sand is mostly quartz), flint, granite, many hard rocks, and some clays.
Simple silicosis is characterized by small rounded nodules scattered throughout the lungs. No single nodule is greater than 9 mm in diameter. Patients with simple silicosis are usually symptom-free.
Complicated silicosis is characterized by nodules that coalesce and form large masses of fibrous tissue, usually in the upper lobes and perihilar regions. In severe cases the fibrotic regions may undergo tissue necrosis and cavitate. Box 27.2 lists common occupations associated with silica exposure.
Box 27.2
Common Occupations Associated With Silica Exposure
•Tunneling
•Hard-rock mining
•Sandblasting
•Quarrying
•Stonecutting
•Foundry work
•Ceramics work
•Abrasives work
•Brick making
•Paint making
•Polishing
•Stone drilling
•Well drilling
Beryllium.
Beryllium is a steel-gray, lightweight metal found in certain plastics and ceramics, rocket fuels, and x-ray tubes. As a raw ore, beryllium is not hazardous. When it is processed into the pure metal or one of its salts, however, it may cause a tissue reaction when inhaled into the lungs or implanted into the skin. The acute inhalation of beryllium fumes or particles may cause a toxic or allergic pneumonitis sometimes accompanied by rhinitis, pharyngitis, and tracheobronchitis. The more complex form of berylliosis is characterized by the development of granulomas and a diffuse interstitial inflammatory reaction.
Other Inorganic Causes.
Box 27.3 lists other inorganic causes of ILD.
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Box 27.3
Additional Inorganic Causes of Interstitial Lung Disease
•Aluminum
•Ammunition workers
•Baritosis (barium)
•Barite millers and miners
•Ceramic workers
•Kalonosis (clay)
•Brickmakers and potters
•Ceramics workers
•Siderosis (iron)
•Welders
•Talcosis (certain talcs)
•Ceramics workers
•Papermakers
•Plastics and rubber workers
Organic Materials Exposure
Hypersensitivity Pneumonitis.
Hypersensitivity pneumonitis (also called allergic alveolitis or extrinsic allergic alveolitis) is a cell-mediated immune response of the lungs caused by the inhalation of a variety of offending agents or antigens. Such antigens include grains, silage, bird droppings or feathers, wood dust (especially redwood and maple), cork dust, animal pelts, coffee beans, fish meal, mushroom compost, and molds that grow on sugar cane, barley, and straw. The immune response to these allergens results in the production of antibodies and an inflammatory response. The lung inflammation, or pneumonitis, develops after repeated and prolonged exposure to the allergen. The term hypersensitivity pneumonitis (or allergic alveolitis) is often renamed according to the type of exposure that caused the lung disorder. For example, the hypersensitivity pneumonitis caused by the inhalation of moldy hay is called farmer lung. Table 27.2 provides common causes, exposure sources, and disease syndromes associated with hypersensitivity pneumonitis.
