hrct lecture

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Practical Approach HRCTJud W Gurney MD FACR

Charles A Dobry Professor of Radiology

University of Nebraska

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HRCT Technique

Maximize spatial resolution

thin collimation

high spatial algorithm

Advantages over chest x-ray

no summation

high contrast

There is no magic with HRCT. The basic premise issimple, maximize spatial resolution by using thethinnest collimation and a high spatial frequencyalgorithm. This use to be 1.5 mm. Moderntechnology has cut the slice thickness in half andwith multi-detector CT any scan can be a highresolution scan. Even without high resolution, CThas inherent advantages over chest radiography.

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Secondary pulmonary lobuleTerminal bronchiole

Pulmonary artery

Septa

Pulmonary vein

Secondary pulmonary lobule

1 - 2.5 cm

Acinus

RB

A quick review of anatomy. One of the buildingblocks of the lung is the secondary pulmonarylobule. Lobules are relatively large: 1 to 2.5 cm, thesize of a good thumbprint. The lobule is fed by aterminal bronchiole and artery, the periphery ispartly septated. In between are the primary lobulesfed by respiratory bronchioles where gas exchangetakes place. Radiographically we can identify thelargest of the arteries and airways and the septa.Veins run in the septa. There are 2 lymphaticsystems, an axial system travels downs the arteriesand airways, terminating at the terminal bronchiolesand a peripheral system that travels along the septaand veins. The yellow and gray rings are thecentriacinar portion of the lobule.

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HRCT dried lung specimen. The larger terminalarteries and airways are clearly visible as are theoccasional septa. However, the respiratorybronchiole and acinus are not resolvable.

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In this fresh autopsy lung, the black pigmentationmarks the centriacinar portion of the lobule.Anthracotic particles (environmental soot) isdeposited in the respiratory bronchioles. Notice theoff-axis location of the respiratory bronchiolescompared to the core bronchovascular structure.

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Diffuse Lung Disease

SarcoidLangerhansIdiopathicDesquamativeCoal workersBagassosisSilicosisDrug reactionAsbestosisLymphangiticErdheim ChesterLymphangiomyomatosisChronic failureFarmer’s lungAnkylosing SpondylitisNeurofibromatosisRheumatoidScleroderma

Hard metal disease

Emphysema

PAP

Aspiration

Gauchers

Sjogrens

LIP

Mushroom workers lung

Methotrexate lung

Respiratory bronchiolitis

BOOP

Periarteritis nodosa

Lupus

Bronchiectasis

Berylliosis

Bronchiolitis obliterans

Alveolar microlithiasis

Metastatic calcification

The number of insults that may give rise topulmonary disease is large anywhere from 100-150.It might seem a hopeless task to sort out thisdifferential. Once when I was doing a locums I cameacross a report that read: “the patient has diffuseinterstitial lung disease. Please stop by my office toreview the list of 150 possibilities”

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Most common diagnoses

1. UIP

2. Silicosis

3. Sarcoid

4. Lymphangitic ca

5. Farmers lung

1. IPF

2. Farmers lung

3. Sarcoid

4. Asbestosis

5. Boop

6. Langerhansgranulomatosis

80% LondonPadley

83% VancouverMatheson

In reality, the number of problems that we deal withare a lot less. For example, this small list of diseasesaccounted for over 80% of the diagnosis at topreferral centers in England and North America.While the spectrum of disease differs slightly, suchas asbestos in England and silicosis in BritishColumbia, the number of diseases one has toconsider is quite small.

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Round up the usual suspects

SarcoidLangerhans granulomatosisIdiopathic pulmonary fibrosisLymphangitic tumorEdemaAsbestosisCollagen vascular diseasesSilicosisFarmer’s lungDrugs

More than 100 entities manifest as diffuse lung disease. Fortunately only 10-20 of these account for about 90% of all diffuse lung diseasethat is assessed by open lung biopsy.

DeRemee Chest 92, 1987

Combining these 2 lists and my own practicalexperience, these 10 processes account for over 90%of what I see in my daily practice. The theme herecomes from the famous scene in Casablanca afterRic has shot the German general. Louie, the Frenchpolice captain, has to make a decision as to whichside he will choose. When his lieutenants comerunning he utters the line; “ the general has beenshot, round up the usual suspects”. This has becomea running joke among the pulmonologists I workwith as this is our approach. When we have a newpatient with interstitial lung disease we look for theusual suspects before considering a more exoticdisorder.

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Sarcoidosis

Common systemic disease unknown etiology

May follow treatment lymphoma

Noncaseating granulomas

Most good prognosis, resolves within 2 years

We will start with sarcoidosis, one of thecommonest of the interstitial lung diseases. Wedon’t know what causes sarcoid, however, onecurious bit of evidence is that sarcoid may followtreatment of lymphoma. It is important to recognizethis possibility as the development of interstitiallung disease and adenopathy in a patient with ahistory of lymphoma is usually equated withrecurrence and not a new disease. The pathologicfinding is the noncaseating granuloma that isprimarily located in the lung lymphatics. Most withsarcoid do well, only a small minority go on todevelop end-stage disease.

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Sarcoidosis

95% abnormal chest radiograph

Symmetric hilar adenopathy

Lung disease (<50%), often worsens with nodalregression

Most have an abnormal chest radiograph. Classicfindings of symmetric hilar adenopathy may befound alone or associated with lung disease. One ofthe distinguishing features in sarcoid is theparadoxical response that as the lung diseaseworsens the nodal enlargement usually regresses.

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Sarcoidosis

Alveolar sarcoid

Airspace masses

Air bronchograms

Usually upper lobes

Hilar adenopathy

The least common form of lung disease is alveolarsarcoid. Typically, there are several large air spacemasses that contain air bronchograms. Usually themasses are larger or more extensive in the upperlung zones. Alveolar sarcoid is usually associatedwith adenopathy as in this case. In addition, thealveolar sarcoid pattern is at high risk forspontaneous pneumothorax.

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Sarcoidosis

Ground glass opacities

Centriacinar nodules

Follow lymphatics (septa,bronchi, blood vessels)

The typical features of sarcoid at HRCT vary.Micronodules are typically located alongbronchovascular bundles, fissures and pleuramirroring the distribution of lymphatics in the lung.

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SarcoidosisFibrosis cuts a swath through lung

“Sherman’s march to the sea”

More advanced fibrosis follows the bronchi andarteries and cuts a swath through the lung from thehilum to the lung periphery. Remember, if you seesomething which looks like General Sherman’smarch to the sea, think sarcoid.

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Langerhans granulomatosis

Probable allergic reaction to cigarette smoke

Granulomas Langerhans cell

25% present spontaneous pneumothorax

2/3rds spontaneously resolve

Next on our list is langerhans cell granulomatosis orhistiocytosis. The etiology is thought to be anallergic reaction to some constituent of cigarettesmoke. The granulomas in histiocytosis contain thelangerhans cell, an antigen processing cell normallyfound in the lung and reticuloendothelial system.Usually affecting young adults, 25% of patients withlangerhans histiocytosis present with a spontaneouspneumothorax. The natural history is unknown butmost spontaneously resolve.

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Mid to upper lobe lung disease

Nodules and cysts

Increased lung volumes

Burned out disease looks like emphysema

The findings of langerhans typically involve the midto upper lung. As we will see shortly, the findingsare combinations of either nodules or cysts. Theearliest findings are thought to be nodules whicheventually evolve into cysts. In contrast to mostinterstitial lung diseases, the lung volumes are eithernormal or increased. Burned out disease may beindistinguishable from emphysema.

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Spontaneous ptx

Biapical coarsereticulonodular pattern

Increased lung volumes

Here is a typical example. Biapical disease with acoarse cystic pattern. The lung volumes are normalto slightly increased. A chest tube on the right wasplaced for a spontaneous pneumothorax.

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Centriacinar micronodules

Respiratory bronchioles

Lung periphery spared

Just like sarcoid, a common pattern at HRCT arecentriacinar micronodules. In contrast to sarcoid,however, the periphery is spared. Judge the lungalong the chest wall and fissues. If there are only ahandful of subpleural nodules then consider theperiphery to be spared.

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Star-fished shapednodules

One feature which I find useful is the shape of thelarger nodules. The may have 3-5 arms or tentacles,similar to the shape of a starfish.

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Nodules cavitate

Aggregate into bizarreshapes

As the nodules get larger they cavitate andeventually aggregate into very bizarre shapes. Thisis distinctive and nearly pathognomonic forlangerhans histiocytosis. This example comes fromthe chest x-ray that we saw earlier. Note that thecystic pattern was not as evident on the chestradiograph, the value of eliminatingsuperimposition.

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Respiratory vs lymphatic nodules

Sarcoidosis Langerhans

In both sarcoid and langerhans cell histiocytosis, oneof the earliest findings are the tiny micronodules. Insarcoid, the granulomatous nodules are locatedwithin the lymphatics and will involve both the axialand peripheral lymphatic systems. This wlll lead tomultiple subpleural nodules along the chest wall andfissures. Langerhans cell granulomatous is a diseaseof the airways. Particles in cigarette smoke depositin the respiratory bronchioles where they incite agranulmatous response. The periphery of the lobulewill be spared and the number of subpleural noduleswill be few. This leads to the concept of arespiratory nodule vs a lymphatic nodule. I find thisconcept useful in formulating a differentialdiagnosis.

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Any patternAny patternDrugs

Nodules, (respiratory)

Nodules, (lymphatic)

Farmers lung

Silicosis

Environment dusts

Reticular, honeycominglLower lobe (periphery)Collagen vasculardisease

Reticular, honeycomgingLower lobe (periphery)Asbestosis

Smooth septalBatwing, dependent lungChronic edema

Irregular septalSpares lobe or lungLymphangitic tumor

Reticular, honeycombingLower lobe (periphery)IPF

Nodules (respiratory)

Bizarre shaped cysts

Upper lobeLangerhans

Nodules (lymphatic)

Fibrotic swath

Upper lobeSarcoid

PatternDistribution

Our first two diseases share many similarities bothin distribution and pattern. However, particularattention should be directed as to whether theperiphery of the lung is involved. Sarcoid has atendency to cut a swath through the lung andhistiocytosis to evolve into bizarre shaped cysts.

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Idiopathic pulmonary fibrosis

Unknown repetitive insult to alveolar wall

Collagen deposition and fibrosis

Gradual onset dyspnea and dry cough

Variable outcome, median survival 5 yrs

Next is IPF. The concept that IPF is an alveolitis isnow discredited with the belief now that there is arepetitive insult to the alveolar wall that results incollagen deposition and fibrosis. Patients usuallyhave the gradual onset of nonspecific symptoms.The prodromal period is unknown, once diagnosedpatients have a median survival of about 5 years.

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Peripheral basilar lungdisease

Reticular lines andhoneycombing

Decreased lung volumes

In contrast to our first two disorders, the distributionof disease is predominantly in the periphery of thelower lobes. The pattern is reticular not nodular.Honeycombing or end stage lung is common.Typically the lung volumes are decreased andparallel the restrictive pulmonary function tests.

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Ground glass opacities

Irregular lines, septalthickening

Honeycombing

Traction bronchiectasis

Ground glass opacities in IPF are nonspecific. Theseopacities may be due to atelectasis or fibrosis whichis below the resolution of the CT scanner. Thelobule may be crisscrossed by a network of finelines. One important characteristic is the presence oftraction bronchiectasis which must be present beforeI can confidently diagnosis IPF.

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Farmers lung

Silicosis

Environment dusts





Reticular, honeycombing


Lower lobe (periphery)IPF




Nodules (lymphatic)

Fibrotic swath

Upper lobeSarcoid

PatternDistribution

IPF is distinctive from the previous disorders,particularly with regards to distribution and pattern.

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Lymphangitic tumor

Carcinoma lung, breast, and GI tract

Permeation of lymphatics by neoplasia

Progressive dyspnea and cough

Prognosis poor

Lymphangitic spread of tumor may arise from manytumors, especially adenocarcinomas. Tumor spreadsto the lymphatics either hematogenously orretrograde from hilar and mediastinal lymph nodes.Lymphangitic spread is a late finding in the naturalhistory of tumor spread and usually portends a poorprognosis.

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Lymphangitic tumor

Not diffuse, usually spareslobe or lung

Lung volumes preserved

Adenopathy or pleuraleffusions

Lymphangitic tumor is usually not diffuse but tendsto spare lobes or even a whole lung. In this example,the left lower lobe was completely spared. Evenwith extensive permeation of lymphatics, lungvolumes are preserved. Patients may or may nothave adenopathy or small pleural effusions.

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Lymphangitic tumor

Nodular thickening axial(bronchovascular) andperipheral (septal) lymphatics

Lymphangitic spread may involve either the axial orperipheral lymphatics or both. In general, axialinvolvement is more common. In this example,lymphangitic spread from colon carcinoma involvedthe right middle lobe only. A characteristic featureof lymphangitic tumor is irregular or nodularthickening of the septa as is noted in this case.

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Edema

Occult edema not uncommon

Extravascular water: ground glass opacities,septal thickening

Orthopnea and dyspnea

Enlarged heart

It might seem surprising that edema is included inthe differential of diffuse lung disease. However, itis surprising how many patients get referred to apulmonary specialist with edema. Most specialiststreat new referrals with a diuretic prior to furtherworkup just in case that their end stage lung maydisappear. The findings of edema: ground glassopacities and septal thickening are identical to thoseof diffuse lung disease. Patients may not give ahistory of orthopena and dyspnea and while anenlarged heart is often found, some may not haverecognizable cardiomegaly.

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Edema

May be chronic, labeled asdiffuse lung disease

Most pulmonologists treatreferrals with ILD withdiuretics before furtherinvestigation

Here is just such a problematic case. Moderatecardiomegaly and mild diffuse interstitial thickeninghad not changed over multiple films obtained overseveral months.

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Edema

Gravitational gradient

Smooth septal thickening

Spares lobules (mosaicperfusion)

One clue to edema is the gravitational distribution.Since many of these patients are upright, groundglass opacities and septal thickening are more severein the lung bases than in the upper lobes. Anothercurious unexplained findings is sparing of lobules asis seen in this patient. From animal experiments, atany given time there are some lobules that are notperfused due to a local autoregulatory mechanism.Starling forces would not affect lobules that are notperfused.

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SeptaLymphangitic tumor Edema

Both lymphangitic tumor and edema involve thesepta. In lymphangitic tumor the septa areirregularly thickened and beaded whereas in chronicedema the septa are smoothly thickened.

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Farmers lung

Silicosis

Environment dusts











Nodules (lymphatic)

Fibrotic swath

Upper lobeSarcoid

PatternDistribution

The distribution of our last two entities is unique. Inaddition there are subtle differences in the septa,irregular and beaded in lymphangitic tumor anduniform and smooth in chronic edema.

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Asbestosis

Pneumoconiosis from fibrous silicates

Latent period 20 - 30 years

Fibrosis + asbestos bodies = asbestosis

High proportion die of lung cancer

Asbestos has been widely used in industry becauseof it’s advantageous fire-retardant properties ininsulation. Asbestosis is only 1 manifestation ofasbestos exposure which includes pleural plaques,diffuse pleural thickening, and mesothelioma. Thepathologic signature in asbestosis is the asbestos orferrugenous body. The asbestos body is an asbestosfiber surrounded by dead macrophages which stainfor iron. Asbestos is carcinogenic and combinedwith smoking, the risk of developing lung cancer ismultiplicative, that is higher than the risk of eitheragent alone.

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Asbestosis

Peripheral and basilar

Irregular reticular opacites

Small lung volumes

25% asbestos plaques

Identical to IPF, asbestosis primarily involves theperiphery of the lower lobes. The pattern is alsoidentical, irregular reticular opacities andhoneycombing. One clue is the asbestos plaque,however, plaques are seen in only 25% of those withasbestosis.

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Asbestosis

Irregular short septal lines

Long parenchymal bands

Centriacinar nodules

Honeycombing

At HRCT, short irregular lines extend from thecentriacinar region to the lung periphery. Longerthicker parenchymal bands may be found in moresevere cases. End-stage honeycombing when severe.

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Collagen vascular disease

Generalized connective tissue disease

Cellular or fibrotic (NSIP or UIP)

Dyspnea

Variable prognosis

Diseases such as rheumatoid arthritis andscleroderma are also associated with diffuseinterstitial thickening. Pathologically, there may be aUIP or NSIP pattern, indistinguishable from IPF.Dsypnea is a common complaint. Prognosis isvariable and life-expectancy is longer with NSIPthan UIP.

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Peripheral basilar

Honeycombing

Decreased lung volumes

Dilated esophagus(scleroderma)

In this example, the peripheral basilar interstitialthickening is identical to IPF. However, the tip-off isthe dilated esophagus in this patient withscleroderma.

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Wide specturm: ground glass,micronodules, honeycombing

NSIP: uniform pattern

Again, at HRCT ground glass opacities are commonbut nonspecific. The key is the distribution and thepresence of intralobular lines or honeycombing.NSIP is a newer pathologic designation, common inthe collagen vascular diseases. NSIP may be eithercellular or fibrotic, a wide gamut. The key in NSIPis that the pathologic fields will be the same from allsampled sites. That implies that the insult occurredat the same time. In contrast, in UIP the biopsyspecimens are inhomogenous with some cellularsections and other noncellular or fibrotic.

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Farmers lung

Silicosis

Environment dusts

Reticular, honeycombingLower lobe (periphery)Collagen vasculardisease

Reticular, honeycombingLower lobe (periphery)Asbestosis









Nodules (lymphatic)

Fibrotic swath

Upper lobeSarcoid

PatternDistribution

For our last 2 disorders, the distribution and patternare identical to IPF. We must be attentive toadditional clues: asbestos plaques or skeletal oresophageal changes in collagen vascular diseases forhelp.

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Environmental dusts

Inorganic - organic dusts

Silica, coal, farmer’s lung

Granulomas, collagen nodules, dust macules

Finally let’s discuss the dusts. Inorganic dusts suchas coal or silica or the organic dusts such as Farmerslung. The pathologic response will vary dependingon the particular dust.

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Silicosis

Upper lobe distribution

Nodules, PMF

Adenopathy, egg-shellcalcification

Similar to sarcoid and langerhans cell histiocytosis,silica and the other round dust particles such as coalconcentrate in the upper lung zones. The pattern isnodular, and the nodules may aggregate into largermasses known as PMF. Particles are removed bylymphatics and thus the nodules are distributed inboth the axial and peripheral lymphatic system. Themediastinal nodes may be enlarged. Particularlywith silica, the enlarged nodes may exhibit egg-shellcalcification.

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Silicosis

Micronodules, lymphaticdistribution

Dorsal distribution

May calcify

HRCT, the nodules are diffuse, identical to that seenin sarcoid. In some, the profusion of nodules may begreater in the dorsal aspect of the lung. Occasionallythe nodules may calcify.

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Farmer’s lung

Often normal

Mid lung distribution

Spares costophrenic angle

Miliary nodules

Farmers lung is our prototypical reaction to organicdusts. Numerous dusts have been shown to cause ahypersensitivity reaction, but Farmer’s lung, due to areaction to the Thermophillic actinomyces organismis the most common. Up to 90% of chest x-rays maybe normal. When abnormal, a fine nodular pattern inthe mid-lung spares the costophrenic angle.

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Farmer’s lung

Centriacinar nodules, respiratory

mid-lungs

Spares costophrenic angle

HRCT may also be normal in up to 50%.Nonspecific ground glass opacities are common.The most characteristic findings include centriacinarnodules often admixed with areas of air trapping.

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chronic farmers lung

idiopathic pulmonary fibrosis

The main differential for chronic farmers lung is IPF.One helpful distinction is involvement of thesubpleural costophrenic lung. IPF is usually mostsevere in the costophrenic angles, whereas this areaof lung is usually less involved in chronic farmerslung.

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Inorganic: upper lobe

Organic: spare cp angle

Environment dusts











Nodules (lymphatic)

Fibrotic swath

Upper lobeSarcoid

PatternDistribution

The environmental dusts are similar to sarcoid, bothin pattern and distribution. Farmers lung mostcommonly involves the mid-lung, and spares thecostophrenic angle.

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Drugs

Often overlooked

Numerous pathologic responses

DAD, hypersensitivity, UIP

May lead to respiratory failure

Lastly, consider drug reaction. These are oftenoverlooked. The number of drugs which canadversely affect the lung is immense. Nearly anypathologic response can be due to drug toxicity. Ifthe offending drug is not removed, it may causerespiratory failure.

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Drugs

Macrodantin: UIP pattern

Add to differential for anydiffuse lung disease

In this patient with macrodanton toxicity, the patternis indistinguishable from IPF.

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Inorganic: upper lobe

Organic: spare cp angle

Environment dusts











Nodules (lymphatic)

Fibrotic swath

Upper lobeSarcoid

PatternDistribution

Our final pattern is that of drug reaction which mayproduce any pattern or distribution that we’ve seenso far. I always add drug reaction into the mix ofany differential diagnosis for diffuse lung disease.

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