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This is inflammation of the uvea which is the vascular coating of the eye which is between the retina and the white or sclera of the eye.
Injury, infections as well as autoimmune disorders can be linked with the development of uveitis, but the exact cause is really unknown.
Symptoms can occur very suddenly as well as rapidly worsen, but in some cases, the symptoms develop very gradually. An individual needs to contact their physician if they believe they have symptoms of uveitis.
Infections such as herpes, cat-scratch disease, toxoplasmosis, syphilis, tuberculosis or West Nile virus. When visiting your ophthalmologist or eye specialist, the physician will more than likely conduct a total eye exam as well as gather a thorough health history. The physician can recommend anti-inflammatory drugs, such as a corticosteroid, to manage uveitis.
If uveitis is triggered by an infection, antiviral drugs, antibiotics, or other drugs can be given with or without corticosteroids so as to bring this infection under control.
Cytotoxic or immunosuppressive agents can become essential if the uveitis reacts poorly to corticosteroids or if it develops severe enough to be a peril to the vision. Vitrectomy which is a procedure to get rid of some of the jelly-like matter in the eye – vitreous – may be desirable both for diagnosis as well as the management of uveitis.
The area of the eye affected by uveitis – either the back (posterior) or the front (anterior) of the uvea can govern how fast the eye heals.
This website is for informational purposes only and Is not a substitute for medical advice, diagnosis or treatment.
Because your feet are so far away from your heart, it takes them much longer to heal than other parts of the body – this is because it takes much longer to circulate blood from your heart to your feet.
Swelling of the feet and ankles is normally caused by a serious condition of either the heart, kidneys, of blood vessels. Tom Corson-Knowles Blog by Tom Corson-Knowles is licensed under a Creative Commons Attribution-ShareAlike 3.0 Unported License. The contents of this Site, such as text, graphics, images, and other material contained on the Site ("Content") are for informational purposes only. Because there are more than 100 separate disorders, it is helpful to group them based on cause, disease associations, or pathology.
As the name implies, the histologic abnormalities that characterize ILD generally involve the pulmonary interstitium to a greater extent than the alveolar spaces or airways, although exceptions exist. Many of the ILDs have similar clinical features and are not easily distinguished on examination.
Most patients with ILD have bilateral inspiratory fine crackles, which usually are most prominent at the lung bases. Signs of pulmonary arterial hypertension with right ventricular dysfunction, such as lower-extremity edema or jugular venous distention, can occur late in the course of any ILD and are not helpful in diagnosing a specific ILD. Examination also can disclose features of underlying connective tissue disease, including active joint inflammation (synovitis), joint deformities, or skin rash. There is considerable variability among the specific diseases in the character and distribution of radiographic abnormalities. The plain chest radiograph and HRCT features of idiopathic pulmonary fibrosis (IPF) are important patterns to recognize because, next to sarcoidosis, IPF is the most common ILD, several other ILDs have a similar appearance, and IPF images are the prototypic pattern of fibrotic injury response in the lung.
In contrast to the fibrotic type of injury, some diseases cause an inflammatory abnormality with a much different radiographic image. Similar to the radiographic findings, among the specific diseases there can be considerable variability in the physiologic abnormalities seen.
Although not commonly pursued, the compliance characteristics of the lungs can be evaluated with an esophageal balloon to measure intrathoracic pressure at various lung volumes.
The three most common types of occupational ILD are asbestosis, chronic silicosis, and coal worker's pneumoconiosis (CWP). Asbestos exposure also can result in benign asbestos pleural effusions (BAPE) or an entity known as rounded atelectasis. The term asbestos-related pulmonary disease may be used to encompass all of these entities, and asbestosis is reserved for patients who have evidence of parenchymal fibrosis.
No medical therapy has been demonstrated to improve or decrease the progression of asbestosis. It is important to recognize the association of silicosis with lung cancer and active tuberculosis.10 Patients with silicosis are at increased risk for lung cancer, and the risk is increased when combined with exposure to tobacco smoke, diesel exhaust, or radon gas. There are no proven therapies for either silicosis or CWP other than eliminating future exposure. Many drugs have been associated with pulmonary complications of various types, including interstitial inflammation and fibrosis, bronchospasm, pulmonary edema, and pleural effusions.11 Drugs from many different therapeutic classes can cause ILD, including chemotherapeutic agents, antibiotics, antiarrhythmic drugs, and immunosuppressive agents (Box 1). Patients must be sensitized by an initial exposure, with subsequent re-exposure leading to acute hypersensitivity pneumonitis or chronic hypersensitivity pneumonitis.
Because the relation between an exposure and the lung disease might not be obvious, a careful systematic occupational, environmental, and avocational history is critical in evaluating patients with ILD. Specific therapies for hypersensitivity pneumonitis are strict antigen avoidance and immunosuppression with corticosteroids in patients with symptomatic or physiologically impairing disease. Although the association between tobacco use and COPD is well known, the relation with ILD is less well appreciated. Approximately 90% of patients with desquamative interstitial pneumonitis and RB-ILD are current or former tobacco smokers.
In any of these disorders, pulmonary involvement can remain undetected until significant impairment is present, because these patients may be inactive because of the underlying connective tissue disease. The pathologic pattern of injury with these diseases is as equally diverse and correlates with the HRCT findings. Corticosteroids are commonly used in managing sarcoidosis, but treatment usually is reserved for patients with marked symptoms or physiologic impairment attributable to the disease.21 Other organs that can require corticosteroid therapy include the heart, uvea (uveitis), and central nervous system (cranial nerve abnormalities). Unfortunately, even after a comprehensive evaluation many patients with ILD do not have a well-defined specific exposure, a systemic illness, or an underlying genetic cause. The majority of patients are older than 60 years, and IPF is extremely unusual in persons younger than 40 years. Transbronchial lung biopsies are often obtained at bronchoscopy during the evaluation of ILD and to identify mimics of IPF such as sarcoidosis and chronic hypersensitivity pneumonitis. The majority of patients die of progressive fibrosing lung disease within 4 years of diagnosis.
The other one half experience stable lung function or minimal decline for months to years, only to have sudden worsening over a few weeks or months leading to death. Nonspecific interstitial pneumonitis (NSIP) is an IIP with diffuse inflammation seen on surgical lung biopsy.32 These patients are on average 7 to 10 years younger than those with IPF, but considerable overlap exists. The prognosis is much better for NSIP than for IPF, and most patients survive 7 to 10 years.
Cryptogenic organizing pneumonia (COP), is the revised nomenclature for bronchiolitis obliterans organizing pneumonia (BOOP). Lymphangioleiomyomatosis (LAM) is a rare disorder of abnormal smooth muscle tissue proliferating around small airways leading to severe obstruction and destruction of alveoli with resultant thin-walled cyst formation.34 All patients are women, although both male and female patients with tuberous sclerosis complex can develop lung pathology identical to LAM termed tuberous sclerosis complex lymphangioleiomyomatosis (TSC-LAM). Dyspnea on exertion and an obstructive ventilatory impairment with a reduced DLCO are almost always present except in very early disease.
Because hypoxemia is common in ILD, supplemental oxygen therapy is often prescribed, although it has not been studied as extensively as in chronic obstructive pulmonary disease.
We favor continuous rather than pulse delivery because the desaturation with activity seen in most patients is not rectified with pulse therapy. As with supplemental oxygen therapy, pulmonary rehabilitation in the management of ILD has not been as well studied as it has in obstructive lung disease. Because many ILD patients are treated with immunosuppressive medications and are at some modest increased risk for the development of infections, patients with ILD should receive a pneumococcal vaccine per the Centers for Disease Control and Prevention (CDC) guidelines and a yearly influenza virus vaccine.
ConclusionThe entities grouped as ILDs are a diverse group of illnesses of varied causation, treatment, and prognosis.
A careful history, paying attention to exposures and systemic diseases, is required to arrive at a correct diagnosis. High-resolution computed tomography scanning and pulmonary function testing are integral to diagnosing and monitoring disease progression. Treatment depends entirely on the disease cause and may include observation, exposure avoidance, or immunosuppression. Elliot TL, Lynch DA, Newell JD Jr, et al: High-resolution computed tomography features of nonspecific interstitial pneumonia and usual interstitial pneumonia. Hunninghake GW, Lynch DA, Galvin JR, et al: Radiologic findings are strongly associated with a pathologic diagnosis of usual interstitial pneumonia.
Schwartz DA, Davis CS, Merchant JA, et al: Longitudinal changes in lung function among asbestos-exposed workers.
Camus P, Bonniaud P, Fanton A, et al: Drug-induced and iatrogenic infiltrative lung disease. Vourlekis JS, Schwarz MI, Cherniack RM, et al: The effect of pulmonary fibrosis on survival in patients with hypersensitivity pneumonitis. Tashkin DP, Elashoff R, Clements PJ, et al: Cyclophosphamide versus placebo in scleroderma lung disease.
Swigris JJ, Olson AL, Fischer A, et al: Mycophenolate mofetil is safe, well tolerated, and preserves lung function in patients with connective tissue disease-related interstitial lung disease. Raghu G, Weycker D, Edelsberg J, et al: Incidence and prevalence of idiopathic pulmonary fibrosis. Hunninghake GW, Zimmerman MB, Schwartz DA, et al: Utility of a lung biopsy for the diagnosis of idiopathic pulmonary fibrosis. Martinez FJ, Safrin S, Weycker D, et al: The clinical course of patients with idiopathic pulmonary fibrosis. Collard HR, King TE Jr, Bartelson BB, et al: Changes in clinical and physiologic variables predict survival in idiopathic pulmonary fibrosis. Richeldi L, Davies HR, Ferrara G, Franco F: Corticosteroids for idiopathic pulmonary fibrosis. Davies HR, Richeldi L, Walters EH: Immunomodulatory agents for idiopathic pulmonary fibrosis.
Collard HR, Ryu JH, Douglas WW, et al: Combined corticosteroid and cyclophosphamide therapy does not alter survival in idiopathic pulmonary fibrosis. Nadrous HF, Pellikka PA, Krowka MJ, et al: Pulmonary hypertension in patients with idiopathic pulmonary fibrosis.
Lettieri CJ, Nathan SD, Barnett SD, et al: Prevalence and outcomes of pulmonary arterial hypertension in advanced idiopathic pulmonary fibrosis. Decorticate posturing, with elbows, wrists and fingers flexed, and legs extended and rotated inward. This normally occurs in the ankles, feet, and legs but it can also affect any area of your body. With diabetes and metabolic syndrome growing at skyrocketing rates, it’s now very common to suffer from swollen legs, feet and ankles due to poor circulation and cardiovascular problems, as well as common injuries. Lecithin Seeds – This is an effective treatment for chronic or long term foot swelling.

Mustard Oil – It has shown that massaging your foot with warm mustard oil will help to relieve swelling and pain in the feet and ankles.
Apple Cider Vinegar – Applying this to the affected area will help to reduce the excess of fluid in your foot or ankle and relieve swelling and pain in the affected body part.
Exercise – This will help by taking pressure off the leg and reducing any swelling you may have. Molasses and Saunf Drink – Boil one or two glasses of water with a half teaspoon of molasses and a tablespoon of saunf. She loves to write about natural health solutions, women health, nutrition, diet and green living.
The Content is not intended to be a substitute for professional medical advice, diagnosis, or treatment.
These disorders are grouped together because of similarities in their clinical presentations, plain chest radiographic appearance, and physiologic features.
Gas exchange is impaired due to ventilation-perfusion (Figure 1) mismatching, shunt, and decreased diffusion across the abnormal interstitium.
However, some diseases, such as sarcoidosis and lymphangioleiomyomatosis, have only decreased breath sounds without adventitious sounds despite markedly abnormal chest radiographs. However, for most ILDs, the plain chest radiograph reveals reduced lung volumes with bilateral reticular or reticulonodular opacities. The plain radiograph and HRCT in IPF reveal bilateral, peripheral and basilar predominant disease with reticulonodular infiltrates, often with honeycomb, cystic changes.
In cellular nonspecific interstitial pneumonia, the predominant abnormality is ground glass without distortion of the lung architecture or loss of volume, as seen in Figure 4. In almost all of the ILDs, the lungs have reduced compliance and require supranormal transpleural pressures to ventilate. Predictable clinical and radiographic abnormalities occur in susceptible patients who have been exposed to asbestos.8 These abnormalities include pleural changes (plaques, fibrosis, effusions, atelectasis, and mesothelioma), parenchymal scarring, and lung cancer. Most patients with asbestosis have had considerable asbestos exposure many years before manifestation of the lung disease.
Unfortunately, severe impairment typically occurs 30 to 40 years after exposure, making almost all patients ineligible for lung transplantation because of age. Occupations that commonly entail exposure to silica include mining, tunneling, sandblasting, and foundry work. Silicosis patients develop active tuberculosis 2- to 30-fold more often than coworkers without silicosis.
In the past, it was assumed that silica dust was responsible for the pulmonary disease seen among coal miners because the clinical and radiographic features are quite similar to those of chronic silicosis.
In patients with significant obstructive impairment or mucus production, inhaled bronchodilators and corticosteroids might relieve some symptoms. There are no distinct physiologic, radiographic, or pathologic patterns of drug-induced ILD, and the diagnosis is usually made when a patient with ILD is exposed to a medication known to result in lung disease, the timing of the exposure is appropriate for the development of the disease, and other causes of ILD have been eliminated.
Patients presenting within 6 months of radiation therapy generally have ground glass abnormalities believed to represent acute inflammation.
Patients with acute hypersensitivity pneumonitis usually present with sudden shortness of breath, chest pain, fever, chills, malaise, and a cough that may be productive of purulent sputum.
Inorganic antigens from vaporized paints and plastics can also lead to hypersensitivity pneumonitis. Elements that strongly suggest a diagnosis of hypersensitivity pneumonitis are exposure to an appropriate antigen and the correct temporal relation of symptoms to the exposure.
HRCT usually demonstrates micronodular central infiltrates in RB-ILD and diffuse ground glass in desquamative interstitial pneumonitis. Patients usually have a significant smoking history and develop cough and progressive dyspnea on exertion.
In patients with mild or moderate disease, lung function can stabilize after smoking cessation, but some patients progressively decline.
However, there is generally poor correlation between the severity of the pulmonary and nonpulmonary manifestations of these diseases. Nonspecific interstitial pneumonitis (NSIP) is an inflammatory injury pattern associated with ground glass on HRCT scan, and organizing pneumonia is seen with patchy consolidated lung on air bronchograms. The Scleroderma Lung Study demonstrated that one year of oral cyclophosphamide modestly improved lung function compared with a modest decline in the control group.
Patients usually present with mechanics hands, consisting of thickened skin and painful fingertip fissures; 50% have Jo-1 antibodies on antinuclear antibody testing. The tissue inflammation that occurs in sarcoidosis has a characteristic pattern in which the inflammatory cells collect in microscopic nodules called granulomas. Less often, the chest x-ray demonstrates parenchymal opacities in the mid lung zone; these may be nodular, reticulonodular, or alveolar. Their ILD belongs to either the idiopathic interstitial pneumonia (IIP) group or to the group consisting of unique pathologic patterns as described by surgical lung biopsy. Risk factors for developing IPF include exposure to smoke, metal dust, farming dust, and hairdressing chemicals. Usual interstitial pneumonitis is characterized by heterogeneous fibrosis most prominent in the peripheral areas, with minimal inflammation. The small biopsies obtained by this route may be able to identify granulomatous inflammation but cannot provide a definitive diagnosis of usual interstitial pneumonitis because this diagnosis requires a piece of tissue much larger than that obtained by transbronchial biopsy. Baseline parameters that predict an increased risk of death include severity of dyspnea, severity of restrictive physiologic defect, reduced DLCO, pulmonary arterial hypertension, degree of fibrosis on HRCT, and Sao2 desaturation on exertion.26 Serial parameters that predict poor survival include worsening dyspnea, FVC, and DLCO. Several PAH agents are under investigation in IPF, but their use outside of trials is not recommended. Immunosuppression with oral corticosteroids and cytotoxic immunosuppressive agents is the primary therapy.
Patients are younger than those with IPF, and they present with acute or subacute dyspnea and cough.
However, many patients have recrudescence after corticosteroid withdrawal and require long-term immunosuppression with cytotoxic immunosuppressive agents.
Patients are typically younger than IPF patients and present with subacute dyspnea and cough. Disease progression is quite variable; some women have steadily worsening lung function during midlife, and some elderly women experience extremely slow decline over many years. Patients with ILD should have arterial oxygen saturation determined at rest and especially during exertion, because many patients with only mild disease desaturate with exertion despite normal saturation at rest.
Pulmonary rehabilitation is important in building aerobic fitness, maintaining physical activity, and improving quality of life.
Enthusiasm for the procedure is tempered by the significant risk of mortality at 1 year (10%-25%) and 5 years (50%-60%). Idiopathic interstitial pneumonias: Usual interstitial pneumonia versus nonspecific interstitial pneumonia. It can be very painful and if not treated right away, can cause permanent damage to your lower limbs.
Put your leg up in front of you so it is elevated and apply an ice pack to the swollen area, or a bag of ice wrapped in a clean towel. Get a slice of cucumber and place it on your foot, wrapping it with a cotton cloth or a bandage.
Place your foot in a pan of warm water and pour in ? a cup of salt to jumpstart the swelling reduction process. It is recommended to rotate your ankle 10 times every 30 minutes to encourage blood flow in the affected area.
This will help to remove any salt that is in your urine and in turn will help to reduce swelling in your foot or ankle. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. First, the diseases are broken down into those with known causes or associations and those of unknown cause.
In the normal state, this space allows close apposition of gas and capillaries with minimal connective tissue matrix, fibroblasts, and inflammatory cells such as macrophages. Exertional breathlessness (dyspnea) and a nonproductive cough are the most common reasons patients seek medical attention. Expiratory wheezing is relatively uncommon, and its presence suggests either airway involvement as part of the primary disease process or concomitant airways disease such as emphysema or asthma. In addition, the central and mid lung zone locations of abnormalities are distinct from IPF. Lung volumes are reduced, as is the diffusing capacity of the lung for carbon monoxide (DLCO).
However, because both emphysema and ILD result in impaired gas exchange, the DLCO is significantly decreased.
Generally, lag time is shorter between the initial asbestos exposure and the development of BAPE (<15 years) than that seen with other manifestations of asbestos exposure. The chest radiograph commonly shows upper lung zone–predominant abnormalities characterized by multiple small nodular opacities in the central lung tissue. This association is especially important in societies with a high incidence of human immunodeficiency virus (HIV) infection, which markedly increases the risk of silicosis-associated active tuberculosis.
However, it is now recognized that CWP and silicosis are the results of distinct exposures.
Exacerbations can be frequent and are treated with antibiotics and systemic corticosteroids. Treatment is avoidance of further exposure and systemic corticosteroids in markedly impaired or declining patients. In comparison, patients who are chronically exposed to low levels of inhaled antigens can develop subtle interstitial inflammatory reactions in the lung that do not result in noticeable symptoms for months to years; these patients present with severe, impairing disease, which can be very difficult to distinguish from IPF.
Numerous established antigens are listed in Table 1, along with the typical source of exposure and the associated syndrome.
Blood samples may be obtained to determine whether there has been an antibody response to certain antigens associated with hypersensitivity pneumonitis (serum precipitins); however, the presence of such antibodies is not sufficient to establish the diagnosis of hypersensitivity pneumonitis because many persons develop antibodies in the absence of disease. However, three types of ILD have a strong association with cigarette smoking: desquamative interstitial pneumonitis, respiratory bronchiolitis associated-interstitial lung disease (RB-ILD), and pulmonary Langerhans cell histiocytosis (PLCH). Spirometry is variable; most patients have significant restriction and variable amounts of obstruction. Stabilization or improvement with oral corticosteroids is described, but overall benefit is unproven.
In some instances, the lung disease overshadows or even predates the other symptoms of the underlying disease. Curiously, those with the highest degree of fibrosis on HRCT improved most, and ground glass or an inflammatory pattern on bronchoalveolar lavage did not predict benefit.
Serum angiotensin-converting enzyme levels and gallium scans are not well correlated with disease activity, and their routine use is discouraged. Patients present with chronic cough and exertional dyspnea, and HRCT demonstrates bibasilar, peripheral reticular abnormalities with focal honeycomb cystic change. Several medications are currently under investigation, including bosentan, imatinib, and pirfenidone.

Type and duration of therapy are guided by disease activity and degree of inflammation on biopsy and ground glass on HRCT. About one third describe an antecedent viral illness; however, no other risk factors are known. A minority of patients develop progressive fibrosis despite aggressive immunosuppression and can be offered lung transplantation. Risk factors for worsening lung function include a significant bronchodilator response and possibly childbearing. Early studies with the immunosuppressant rapamycin, which also inhibits LAM cell proliferation, have been promising, and larger trials are under way. Although studies are limited, supplemental oxygen delivered via nasal cannula can prevent resting hypoxemia and allow greater exertion before desaturation. In motivated patients, transtracheal delivery of supplemental oxygen increases the efficiency of delivery and improves cosmesis.
We encourage all of our patients to enroll in outpatient pulmonary rehabilitation and to continue maintenance therapy. Findings on examination are often limited to the chest in the form of fine inspiratory crackles. Never disregard professional medical advice or delay in seeking it because of something you have read on this site! Diseases with known causes are further classified based on specific exposure, association with systemic disease, or association with a known genetic disorder. The interstitium supports the delicate relation between the alveoli and capillaries, allowing efficient gas exchange. Together, these physiologic impairments lead to the exercise intolerance seen in all of the ILDs.
However, sputum production, hemoptysis, or wheezing are helpful in classifying the disease. Occasionally, wheezing is a clue to a particular diagnosis, such as sarcoidosis, which can involve the airways as well as the interstitium. Note the overall volume loss and poorly demarcated pleural-parenchymal borders along the hemidiaphragms and heart, indicating parenchymal abnormalities extending to the pleura. Understanding these two patterns as ends of an extreme, we shall see how the clinician is able to evaluate other diseases in a similar context.
This reduction in diffusing capacity reflects a pathologic disturbance of the alveolar-capillary interface. Asbestos exposure and cigarette smoking, however, act synergistically to greatly increase the risk of cancer.
Patients report very slowly progressive dyspnea on exertion9 and have crackles on lung examination.
These nodules can slowly coalesce into large masses known as progressive massive fibrosis (PMF). Simple CWP, characterized by multiple small nodular opacities on the chest x-ray film, is asymptomatic. Likewise, the absence of detectable antibodies does not rule out the diagnosis of hypersensitivity pneumonitis because the culprit may be an antigen that is not included in the blood analysis. As with other toxic exposures, complete avoidance of all smoke is important for these patients.
Patients with progressive disease despite avoidance of all smoke exposure may be offered lung transplantation. At the other end of the pathologic response spectrum is usual interstitial pneumonitis, which is associated with reticular opacities and honeycomb cystic fibrosis on HRCT scan. Unfortunately, after one year off immunosuppressive therapy, the cyclophosphamide-treated patients worsened and were indistinguishable from the untreated control group. As would be expected with these inflammatory patterns of injury, patients usually benefit from immunosuppression. Sarcoidosis often follows a benign course without symptoms or long-term consequences, and it can spontaneously remit.
Pulmonary physiology may be normal, restrictive, obstructive, or mixed and can include a reduced DLCO. When there is active disease, acutely ill patients are treated with prednisone, and long-term immunosuppression is with methotrexate and cyclophosphamide, although infliximab is emerging as a useful agent in some patients. Pathologic NSIP is not a unique pattern and can often be seen in connective tissue disease or hypersensitivity pneumonitis; a thorough investigation for these should be undertaken to rule out these alternative diagnoses.
Organizing pneumonia is not a unique pathologic pattern and is often associated with connective tissue disease. Other important disease manifestations include pneumothorax from a ruptured subpleural cyst, occasionally associated with air travel. These benefits can improve quality of life and potentially ward off development of pulmonary arterial hypertension, although further studies are needed. However, patients must be chosen carefully because of the need for frequent care and the risk of mucus desiccation and rare hemorrhage.
Patients treated with certain specific immunosuppressive regimens should receive Pneumocystis prophylaxis.
Comorbidities such as gastroesophageal reflux disease, common in a number of ILDs, preclude lung transplantation due to the increased risk of chronic rejection and death. The most common chest radiograph finding is diffuse reticular or reticulonodular infiltrates with reduced lung volumes. Dab the area until the towel dries and then repeat this process for twenty minutes, twice a day. Unfortunately, if the initiating injury or abnormal repair from injury is not halted, progressive tissue damage can lead to worsening physiologic impairment and even death.
If the patient also has prominent nonrespiratory symptoms, such as myalgia, arthralgia, or sclerodactyly, ILD might be the result of underlying connective tissue disease. Figure 3 shows an HRCT image of IPF, with distortion of the lung architecture and traction bronchiectasis, especially at the lung bases.
In a patient with a history of asbestos exposure and a bloody pleural effusion, the major differential diagnostic concern is malignant pleural effusion, particularly associated with mesothelioma, another asbestos-related disease.
Cough and shortness of breath do not develop unless the disease progresses to PMF similar to that seen in silicosis. In contrast, dyspnea that develops more than 6 months after therapy typically appears as densely fibrotic tissue within the radiation port. In RB-ILD, physiologic stabilization and occasionally even improvement can occur after abstinence from tobacco. On chest examination, rales, wheezing, or even a pleural rub may be heard because of the varied patterns of lung involvement in these disorders. It appears to respond little to immunosuppression, although long-term controlled studies are lacking. Many hypothesize that to preserve any lung function gained by cyclophosphamide, continued immunosuppression, usually with mycophenolate, is necessary. The classic COP patient presents after having failed to improve despite several courses of antibiotics. Most patients respond well to oral corticosteroids; a minority require long-term immunosuppression. Unilateral or, less commonly, bilateral chylothorax is seen in about one third of patients.
Pulmonary function testing usually reveals restrictive physiology and decreased diffusion capacity; however, other patterns can be seen. Using this organizational scheme, one can perform a careful and complete history, working toward an accurate diagnosis and appropriate therapy. If the exposure persists or if the repair process is imperfect, the lung may be permanently damaged, with increased interstitial tissue replacing the normal capillaries, alveoli, and healthy interstitium. As predicted by the plain radiograph, the abnormalities are strikingly located in the subpleural and dependent areas of the lung. The clinical course of BAPE is that of spontaneous resolution, often with recurrences, and treatment is drainage to alleviate symptoms. The chest x-ray examination reveals bilateral lower-zone reticulonodular infiltrates similar to those seen in IPF. On CT examination, a straight line indicating the margin of radiation is often evident, as seen in Figure 5. The pathologic pattern is unique; the hallmark Langerhans histiocytes are seen in groups of star-shaped nodules, with destruction of adjacent lung tissue. HRCT demonstrates predominant ground glass abnormalities in cellular NSIP and both ground glass and fibrotic changes in fibrotic NSIP. Diagnosis occasionally requires surgical lung biopsy, especially if the clinical and radiographic features are uncertain, because small areas of organizing pneumonia can be seen in a variety of inflammatory and fibrotic disorders on transbronchial lung biopsy. Therapy depends on the underlying disease and may consist of immunosuppressive drugs and avoidance of disease-inducing exposures.
Ground glass abnormalities, increased attenuation of the lung tissue without distortion of the underlying blood vessels or bronchi, are absent or minimal in classic IPF. Rounded atelectasis typically manifests as a pleural-based parenchymal mass that may be mistaken for carcinoma.
With an appropriate exposure history, the presence of radiographic pleural plaques or rounded atelectasis can indicate asbestos as the cause of the ILD, although neither of these findings is required for establishing the diagnosis. Some patients with abnormal chest radiographs report few, if any, symptoms and can have normal lung examination and pulmonary function tests. Although PLCH is pathologically similar to childhood LCH, the adult form does not typically involve bone and is not proven to respond to chemotherapy, as the childhood form does. Given that there are significant clinical and radiographic overlaps between fibrotic NSIP and IPF, surgical lung biopsy is often required to distinguish these two. Treatment with a low-fat diet or blocking gut fat absorption is usually ineffective, and pleurodesis is required. Pleural disease and significant lymphadenopathy are not seen, although up to two thirds of IPF patients have mild mediastinal adenopathy.5 As the burden of disease increases, the chest x-ray examination can reveal multiple tiny cysts in the most markedly involved regions.
The characteristic computed tomography (CT) features, however, such as evidence of local volume loss, pleural thickening, and the comet tail appearance of bronchi and vessels curving into the lesion may be used to help distinguish rounded atelectasis from carcinoma.
Unfortunately many patients are impaired and have mixed restrictive and obstructive impairments with reduced diffusion capacity. This cystic pattern, called honeycombing, reflects end-stage fibrosis and is a feature of many end-stage ILDs.
The physiologic impairment can remain stable or, if PMF occurs, can progress even in the absence of continued exposure.

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