Radiology Chest

Chronic pulmonary thromboembolic disease: lucent areas are typically much more extensive than the ground-glass areas. Small subpleural nodules may be present, representing infarcts.

"Mosaic attenuation," with attenuated vessels in the relatively lucent areas and relatively large vessels in ground-glass areas.

1. Same as for acute consolidation, BUT pulm edema more common cause, and PNA is more commonly atypical such as viral or PCP 2. Same as chronic consolidation (BOC) plus HSP (Esp in subacute phase - ground glass + centrilobular nodules + mosaic attenuation) plus alveolar proteinosis (idiopathic protein filing of alveoli w CENTRAL distributioN)

1. Ddx for ACUTE GGOs? 2. DDx for CHRONIC GGO?

1. Big arrows: GGOs in periphery, small arrows: faint centrilobular nodules. Can also see bronchial wall thickening. Expect findings to be diffuse. 2. RB-ILD, mainly when findings in upper lung zones. Usually in smokers who have many decades of smoking hx. Tx = smoking cessation 3. Then they have DIP (end of the spectrum of RB-ILD to DIP)

1. What are the arrows pointing to? 2. What is this? (40y smoking hx) 3. What if this person develops diffuse and uniform ground-glass opacities?

1. surrounds the bronchoarterial bundles 2. located within the alveolar walls 3. between the pleura and lung in continuity with the interlobular septa

3 components of the pulmonary interstitium - where are they?: 1. Axial or bronchovascular 2. parenchymal or intralobular 3. peripheral

predominantly peripheral consolidation (hollow arrow, "photographic negative" of pulmonary edema) and small bilateral pleural effusions (straight arrows). Opacities resolve from the periphery, leaving lines (inner edge) paralleling the chest wall. Acute eosinophilic pneumonia (AEP) is an idiopathic acute febrile illness with rapid onset respiratory failure, due to pulmonary eosinophilia. Consider AEP if a patient with suspected hydrostatic edema is nonresponsive to diuresis. Always consider specific causes of eosinophilic lung disease, such as drugs, parasitic infestation, and fungal infection. Tx: roids

31-year-old female patient with 6 months of cough; blood eosinophils 48%.

Pulmonary Langerhans cell histiocytosis occurs almost exclusively in young and middle-aged adult smokers and is characterized by upper lung zone predominant nodules, cavitary nodules, and cysts. As the disease progresses, the cysts increase in number, enlarge, and develop irregular shapes while the profusion of nodules diminishes. Patients may develop or even present with spontaneous pneumothorax. Smoking cessation leads to variable results: some patients improve, some patients stabilize, and others progress

36-year-old male current smoker with worsening cough and dyspnea. (cavitary nodules seen on different slice)

GGOs in upper peripheral lung = eosinophilic PNA

37 year old male w asthma

In a potentially immunocompromised patient, opportunistic viral bronchitis and bronchiolitis are important considerations. CT with thin sections may enable identification of small airways diseases when chest radiographs are unrevealing. Attention should be paid to bronchial wall thickness and airway lumens; airway lumens may be opacified with cellular inflammatory exudate. When bronchioles are involved, so-called cellular bronchiolitis, centrilobular opacities in the form of tubular, branching, and tree-in-bud opacities may be present. This patient was diagnosed with respiratory syncytial virus (RSV) bronchiolitis. Other viral agents that should be considered include Cytomegalovirus (CMV) and parainfluenza.

38-year-old male patient with leukemia, fever, and cough.

Bronchiolitis obliterans (BO) is the concentric luminal narrowing of the membranous and respiratory bronchioles secondary to submucosal and peribronchiolar inflammation and fibrosis without intraluminal granulation tissue and polyps. A mosaic attenuation is seen 50% of the time. The unilateral form is known as Swyer-James syndrome (unilateral hyperlucent lung). Etiologies include cryptogenic, postinfectious (viral), toxic fume inhalation, bone marrow and lung transplantation rejection, rheumatoid arthritis, inflammatory bowel disease, and drug toxicity (penicillamine). This occurs in up to 50% of patients with lung transplants. Ten percent of patients are receiving allogeneic bone marrow transplants from graft-vs.-host disease.

41-year-old female post lung transplantation in a patient with cystic fibrosis.

Silicoproteinosis is a variant of silicosis that presents with perihilar ground-glass opacities with septal thickening that resembles alveolar proteinosis. Occupational exposure will help the etiology. Hilar/mediastinal lymphadenopathy is common. Again, this disease progresses rapidly over months. It can later evolve into fibrosis with severe architectural distortion, bullae, and pneumothorax.

41-year-old male patient who works as a sand-blaster presents with acute shortness of breath.

Broncholith

42-year-old female patient with persistent left lung opacity on chest radiography.

Kaposi's sarcoma: Flame shaped nodules/opacities in peribronchiovascular distribution

44 year old male

Numerous irregular nodules, upper lobe predominant, in a typical perilymphatic distribution along the pulmonary fissures (white arrow) , peripheral pleural surface (black arrow), and around bronchovascular bundles (hollow arrow) --> Sarcoidosis, even when there is not bilateral mediastinal LNs.

44-year-old male patient presents with cough and worsening dyspnea on exertion.

Finger-in-glove mucoid impaction and bronchiectasis = ABPA - Typical pt: Asthma or CF (bronchiectasis in 3 or more lobes in asthmatics is highly suggestive of ABPA) - Hypersensitivity (IgE and eos elevated) to ABPA antibody - Usually affects upper lobes - Tx: oral roids

44-year-old male patient with asthma.

DIP - Macrophages filling airspaces --> groundglass, mostly basal - Small cysts (in 80%) As opposed to RB-ILD, which causes faint, ill-defined centrilobular nodules in UPPER lung zones

45-year-old female patient with 25-year history of smoking and worsening shortness of breath.

NSIP: Lower lobe predominant peribronchovascular ground-glass opacities with subpleural sparing and reticular interstitial opacities.

47 year old w no smoking hx and gradual onset of dyspnea. What is this?

Another example of ABPA

47-year-old male patient with intermittent episodes of a cough that is sometimes productive with thick mucus.

Pathophys: abnormal proliferation of smooth muscle-like cells in the lungs Assoc w: Tuberous sclerosis (more common than spont LAM) Almost exclusively seen in females Other manifestations: mediastinal and retroperitoneal lymphangiomas and renal angiomyolipomas - VEGF-D levels often elevated in serum, can be used to confirm diagnosis

48-year-old female patient with progressive dyspnea on exertion.

UPPER lobe predominant Well-defined, rounded (<1cm), and coalescent nodules in a perilymphatic distribution (Coalescence of subpleural nodules leads to formation of pseudoplaques) + R paratracheal node enlargement (these can also get calcified) --> Silicosis or coal workers pneumonitis (hard to distinguish radiographically) The nodules in sarcoidosis are also upper lobe predominant but would be more irregular Nodules can begin to coalesce into large fibrotic opacities, termed complicated pneumoconiosis or progressive massive fibrosis (PMF) --> pts get symptomatic.

49 year old male w no symptoms. What is it? (describe the findings) What has a similar distribution? What happens this progresses?

basal, peripheral, and peribronchial consolidation with air bronchograms (, #1, 3-4). Surrounding ground-glass opacity (, #2, 4) is present in some areas. = Cryptogenic organizing PNA Causes are numerous and include infection, drug reaction, connective tissue disease, hemorrhage, and radiation Tx: Steroids (pt might still get progressive pulmonary fibrosis) COP waxes and wanes as pts are treated in vain for recurrent PNA

50-year-old female patient presents with 1 week of nonproductive cough and worsening dyspnea, with fever and recurrent pneumonia.

Tree-in-bud opacities, as seen here, are the hallmark of infectious bronchiolitis. Diffuse tree-in-bud opacities favor infection bacteria, such as Mycoplasma, or respiratory viruses, such as respiratory syncytial virus (RSV). Aspiration bronchiolitis can also cause tree-in-bud opacities, which are usually located in the dependent portions of the lungs. Bronchiectasis and bronchial wall thickening in the same distribution may also be present. In patients with rheumatoid arthritis, chronic tree-in-bud opacities may be the manifestation of follicular bronchiolitis (peribronchiolar lymphoid follicles, usually with germinal centers). Rare causes of (vascular) tree-in-bud opacities include endovascular metastases (especially renal cell carcinoma) and vascular granulomatosis from intravenous drug abuse with crushed oral medications.

51-year-old female patient with cough, wheeze, and fever.

Straight arrows: hyperattenuation of lung parenchyma (from pigment-laden macrophages in smokers) Curved arrows: very SMALL cysts = DIP (desquamative interstitial PNA)

52-year-old male chronic smoker with known emphysema undergoing CT. Describe findings. What is this?

stage 4 sarcoidosis (extensive parenchymal fibrosis) is the presence of generally symmetric upper lobe, large opacities ("progressive massive fibrosis"). Also: Lymph node calcs, curved arrows showing patent bronchi (need to make sure there is no mass causing obliterative malignancy. It is sometimes not possible to distinguish complicated inorganic dust pneumoconiosis from the correct answer in this case on radiographic grounds alone. When many adjacent small nodules are present, particularly in posterolateral and apical subpleural locations (pseudoplaques), this entity is favored.

56-year-old female patient with a history of "lung fibrosis." - Alternative dx: What if there were pseudoplaques?

Again, GGOs w subpleural sparing + reticular opacities with traction bronchiectasis that is out of proportion to the reticular opacities

58-year-old male patient with a history of polymyositis presents with cough, fatigue, and progressive shortness of breath. Patient denies a history of smoking.

Spiculated margins + lots of fat in these = chronic exogenous lipoid PNA from chronic ingestion of oily materials When nonresolving presumed bacterial PNA, consider these: tumor, noninfectious organizing pneumonia, aspiration pneumonia, eosinophilic, and lipoid pneumonia.

60-year-old female patient presents for evaluation of nonresolving pneumonia. On lung window, these look like spiculated masses What dx to consider when pneumonia does not resolve?

Areas of panlobular emphysema may be relatively difficult to perceive as discrete and circumscribed bullae are not evident. An important observation is the substantive attenuation or "absence" of pulmonary vessels in hypoattenuating regions of lung parenchyma. If expiration images are obtained at residual volume, look for air trapping in these regions. If such findings are extensive in the lower lung zones, consider alpha-1 antitrypsin deficiency as an etiology for the emphysema.

62-year-old male patient with an obstructive pattern on pulmonary function testing.

Mesothelioma

75 year old male w SOB

extensive basal predominant ground-glass opacity and foci of mild-to-moderate traction bronchiectasis = NSIP basal-predominant ground-glass opacity, with or without reticulation, and traction bronchiectasis. Subpleural sparing, when present, is highly suggestive of this pattern of diffuse lung disease. Honeycombing is very uncommon with NSIP but can develop with advanced disease. Associated w collagen vascular disease, especially systemic sclerosis, scleroderma, mixed connective tissue disease, and polymyositis/dermatomyositis. Other causes include drug reaction, familial fibrosis, and hypersensitivity pneumonitis.

86-year-old female patient with chronic dyspnea.

Not seen in obstructive atelectasis. Can be seen in subsegmental atelectasis (caused by obstruction of small peripheral bronchi from secretions)

Air bronchograms are seen in what kind of atelectasis and not seen in what other kind?

paucity of vessels in the left lower lobe and Segmental bronchi show mild cylindrical bronchiectasis = bronchiolitis obliterans - Reasonable alternative: brochial atresia

Air trapping in left lower lobe. - What about if a bronchocele or mucoid impaction in an obstructed bronchus

1. Volume loss: displaced fissures, vascular crowding 1. Elevation of diaphragm, rib crowding, mediastinal shift/hilar displacement, overinflation of adjacent side or of contralateral lobes

Atelectasis: 1. Direct signs (2) 2. Indirect signs

1. Endobronchial spread of TB or atypical mycobacteria (acid fast but do NOT cause TB, e.g. Mycobacterium avian-intracellulare - typical pt is low grade infection in old lady) 2. BronchoPNA (infectious PNA spread via airways 3. Atypical PNA (Esp mycoplasma)

Centrilobular nodules INFECTIOUS ddx:

1. HSP (Type 3 hypersens rxn; subacute phase has CL nodules) 2. Hot tub lung: Inhale atypical mycobacteria 3. RB-ILD - Respiratory bronchiolitis interstitial lung disease = inflammatory run to cigarette smoke, mediated by PIGMENTED MACROPHAGES 4. Diffuse panbronchiolitis - chronic inflammatory d/o: lymphoid hyperplasia of walls of bronchioles --> bronchiolectasis 5. Silicosis - upper lobe centrilobular and perilymphatic nodules

Centrilobular nodules INFLAMMATORY ddx: 1. Type 3 hypersensitivity 2. S/p hottub 3. Smoker 4. Asian 5. Upper lobe predominant

1. Blockage of centrilobular bronchiole, less commonly of CL artery 2. See multiple small nodules @center of SPN. NEVER extend to the pleura 3. Both/either 4. Up to 1cm

Centrilobular nodules: 1. Caused by what? 2. See what on CT? Nodules never extend to the xxx 3. Solid vs GGO nodules? 4. Size?

BOC: 1. Bronchioaleolar Ca (mucinous subtype of adenoCa) 2. Organizing PNA - response to injury where granulation polyps fill distal airways --> rounded and nodular consolidation 3. Chronic eosinophilic PNA - eosinophils cause alveolar filling in upper lobes

Chronic consolidation ddx 1. Ca 2. Rounded and noudular consolidations 3. Upper-lobe inflammatory process

Ddx: 1. PNA 2. Pulm hemorrhage 3. ARDS (noncardiogenic pulmonary edema 2/2 increased capillary permeability) 4. Pulmonary edema (uncommon)

Consolidation = ? Ddx for acute consolidation

1. LAM 2. Pulm langerhans cell histiocytosis 3. Centrilobular emphysema 4. LIP

Cystic lung lesions ddx: 1. uniform distribution of thin-walled lung cysts 2. nodules and irregular-shaped cysts that predominate in the upper lobes, classically sparing the extreme lung bases, particularly the costophrenic sulci. 3. no perceptible walls and predominate in the upper lungs 4. scattered small basal predominant lung cysts, often associated with scattered nodules and patchy ground-glass opacities

Anything that dilates the pulmonary veins. Ddx same as for ddx for CENTRAL GROUND GLASS (HEAA)

Ddx for SMOOTH interlobular septal thickening:

Crazy paving = GGO + ILS (interlobular septal) thickening Alveolar proteinosis.Pneumocystis jiroveci pneumonia.Organizing pneumonia.Bronchioloalveolar carcinoma, mucinous subtype.Lipoid pneumonia, an inflammatory pneumonia caused by a reaction to aspirated lipids. Acute respiratory distress syndrome.Pulmonary hemorrhage.

Ddx for crazy paving

1. Pulmonary edema 2. Alveolar hemorrhage 3. PCP 4. Alveolar proteinosis (cray paving shown in image)

Ddx for diffuse but CENTRAL predominant ground glass

Anything that infiltrates peripheral lymphatics (MC lyphangitic carcinomatosis i.e. tumor spread thru lymphatics, and sarcoidosis)

Ddx for nodular/irregular/asymmetric septal thickening (2)

1. Organizing PNA 2. Chronic eosinophilic PNA 3. Atypical/viral PNA 4. Pulmonary edema (peripheral TENDS to be noncardiogenic, such as edema triggered by drugs)

Ddx for peripheral GGO or Consolidation

parenchymal bands (curved -->), interlobular septal thickening (white -->), and nodular densities (hollow white -->) within both lung bases are demonstrated. Calcified pleural plaque formation (hollow black -->). --> Asbestosis

Describe the findings

chronic bronchitis: Productive cough that is usually present daily for 3 months in a row, with those periods occurring for at least 2 consecutive years.

Diagnostic criteria for chronic bronchiolitis:

1. Chronic and acute eosinophilic PNA (CEP and AEP; both tx by steroids), Loeffler syndrome, idiopathic hypereosinophilic syndrome 2. ABPA, parasitic infections, Churg-Strauss, Drug reactions

Eosinophilic PNA: 1. List those of unknown cause 2. List those of known cause

A pattern of mosaic attenuation from air-trapping in conjunction with poorly defined centrilobular nodules is characteristic of hypersensitivity pneumonitis. Patients generally respond to cessation of exposure to the offending antigen and corticosteroid therapy. With recurrent exposure, some patients may develop lung fibrosis.

Expiratory CT. Subtle nodules on other slices 61-year-old female patient with cough, dyspnea, intermittent fever, and mild weight loss.

- Partial filling of alveoli, alveolar wall thickening, or atelectasis - Yes, can still have air bronchograms. Main difference is that you can see the blood vessels whereas w consolidation you cannot

Ground glass opacities are due to (3) - Air bronchograms present?

ARDS from drug toxicity (if this was in an immunocompromised pt w respiratory symptoms, consider PCP cus it can look similar)

Hx of lung Ca s/p erlotinib and radiation therapy. Dx?

Pseudomonas (CF)

MC organism isolated from young woman w this CXR

a UIP (usual interstitial pneumonitis) or NSIP (nonspecific interstitial pneumonitis) pattern

Most scleroderma patients have interstitial fibrosis in What 2 patterns?

A1AT deficiency --> will also get cirrhosis Consider lung transplant

Nonsmoker in 40s w lower lobe emphysema

Pneumomediastinum

Pt w asthma

PCP

Pt w low CD4 count and this =

Alveolar edema (these are GGOs)

Pt w pulmonary edema. What is the arrow pointing to?

UIP (usual interstitial pneumonitis), NSIP (nonspecific interstitial pneumonitis), or OP (organizing pneumonitis) pattern RA may or may not have unilateral pleural effusion or pleural thickening, rheumatoid nodules are rare and seen in ≤ 5% of patients with RA.

Rheumatoid arthritis (RA) is characterized as subpleural basal predominant fibrosis in what patterns?

1. Centrilobular artery (faint dot on CT) and central bronchus (can't see on CT) 2. Veins and lymphatics 3. InterLOBULAR septa --> thickening on CT = enlargement of venous or lymphatic spaces 4. 12 5. 1-2.5cm

Secondary pulmonary lobule 1. Each SPL has x and x in center 2. x and x collectiont at periphery 3. x encases each SPL (thickening = ?) 4. How many acini per SPL 5. SPL size

centrilobular

Smoking usually leads to what kind of emphysema?

Airway-dominant COPD phenotype, rather than emphysema-dominant COPD: substantial bronchial wall thickening (a visual assessment that the bronchial wall area comprises a disproportionately high percentage of the total bronchial area) without bronchial dilatation.

Spirometry on this smoker shows expiratory airflow obstruction, not significantly diminished after use of bronchodilator. What is present?

Chest radiographs

Staging of sarcoidosis is based on what?

When a pattern of mosaic lung attenuation is present and the regions of relatively low attenuation contain narrowed blood vessels, 2 pathophysiologic states should be considered: obstructive small vessel and obstructive small airways disease. If there is air trapping, --> Constrictive bronchiolitis: Potential causes of bronchiolitis obliterans should then be considered.

There's air trapping on expiration

Circumferential thickening of trachea w ulcer formation and tracheal luminal narrowing

Typical features of Wegener's when the airway is involved?

Silicosis - coal worker pneumoconiosisCorrect: Exposure to coal dust or free silica is the cause of silicosis. Silicosis typically develops after 20 years of exposure. Large opacities greater than 1-2 cm in size are seen in silicosis. It begins in the periphery of the lung. It will have a posterior location on lateral radiograph or CT. It is difficult to distinguish from sarcoidosis. It develops in upper lobes and is associated with bronchial distortion and upper lobe volume loss. Small perilymphatic nodules are usually present. Cavitation may occur from necrosis or infection, especially when greater than 5 cm. Punctate calcifications are common in conglomerate masses. Paracicatricial emphysema is common, peripheral to the conglomerate mass (as can be seen in this case). There is an increased risk of lung carcinoma, independent of cigarette smoking. SarcoidosisReasonable Alternative: Conglomerate fibrosis is difficult to distinguish from silicosis. It is upper and mid lung zone predominant. Air bronchograms are usually present. It has associated traction bronchiectasis, architectural distortion, and volume loss. Punctate or coarse calcification is frequently present. Perilymphatic nodules are typically present. Paracicatricial emphysema is common, peripheral to the conglomerate mass. Mediastinal and bilateral hilar lymphadenopathy is often present. It may be calcified (solid or "egg shell"). Honeycombing is less common than with other end-stage lung diseases. Basal sparing is typical.

WHat is this? 63-year-old male patient who was short of breath. There are punctate calcifications in these hyperdense areas

drug toxicity, asbestosis, collagen-vascular disease (especially rheumatoid arthritis), and rarely, inflammatory bowel disease.

What are some things other than IPF that can cause UIP?

Anterior segmental right upper lobe bronchus - has horizontal course and can be seen en face here.

What bronchus is this

GGOs superimposed on interstitial thickening sharply demarcated from normal lung = crazy paving. Could be many things (like edema), but mainly think of pulmonary alevolar proteinosis. Tx w BAL

What could this be if it's very widespread? Tx?

Circumferential thickening of trachea w possible calcs

What does tracheal amyloidosis look like?

LAM. Assoc w Chylothorax and recurrent pneumothorax

What is associated w this disease?

"reverse halo" or "atoll" sign associated with a focus in the right middle lobe = ring of consolidation around ground glass = sign of COP (seen in 10-20% of COP cases)

What is the sign called w the curved arrow?

Acinar nodules are poorly marginated pulmonary nodular opacities that measure 5-10 mm. Acinar nodules may be present in the setting of alveolar hemorrhage, alveolar edema, bronchopneumonia, aspiration, and tuberculosis.

What is the typical size of acinar nodules in the lungs?

Intermediate stem line: thin vertical line formed by the posterior walls of the right mainstem bronchus and bronchus intermedius. It is visible on 95% of lateral chest radiographs. The normal intermediate stem line thickness is less than or equal to 3 mm.

What is this line?

SCC of trachea

What is this most likely?

Black arrows: subpleural curvilinear opacities, parallel to the chest wall and within 1 cm of the pleura. Hollow white arrows: interlobular septal thickening Hollow black arrows: calcified pleural plaques --> asbestosis

What is this?

Hilar mass. You can see normal pulmonary artery through it ("HILAR OVERLAY SIGN")

What is this?

Left atrial appendage

What is this?

Right atrial appendage

What is this?

UIP subpleural and basal-predominant reticulation with honeycombing and no atypical features permit a confident diagnosis of usual interstitial pneumonia - Expect to also see traction bronchiectasis UIP can be diagnosed w confidence if you DON'T see these other things: upper- or mid-zone predominant disease, the extent of ground-glass opacity exceeds that of reticulation, lobular air trapping (bilateral, 3 or more lobes), extensive consolidation, diffuse non-honeycomb lung cysts, and profuse micronodules (especially in the mid and upper lungs).

What is this?

UIP aka Idiopathic pulmonary fibrosis: - subpleural reticular opacities and honeycombing with traction bronchiectasis apicobasal gradient (findings increase in severity toward the lung bases), and the lung is heterogeneous, with areas of fibrosis alternating with areas of normal lung.

What is this?

irregularly-shaped cystic spaces in the upper lung zones , located about proximal bronchovascular bundles (hollow -->), and multiple subcentimeter cavitated lung nodules, primarily found in the lower lung zones (curved -->)

What is this?

CF (upper lobe predominant bronchiectasis). Assoc w fatty atrophy of pancreas Diffuse, upper lung preponderant bronchiectasis and bronchial wall thickening is seen in this diagnosis. Mucus plugging is seen in airways; centrilobular or tree-in-bud opacities. Air-trapping or mosaic lung attenuation is seen in this condition. Hyperinflation is also seen. Recurrent areas of consolidation are also seen; pneumonia or atelectasis distal to secretions in airways. - Kartagener - ABPA (calcium oxalate makes some secretions bright on CT)

What is this? - What about if pt has sinus issues and lower lobe predominant bronchiectasis? - What about if pt has asthma?

Eggshell calcs - think silicosis - Usually develops after 20 years of exposure - Talcosis has smaller nodules (<1mm), and panacinar emphysema in lower lobes - In contrast, sarcoidosis calcs of LNs are central and smudgy, not eggshell (50% of sarcoid pts have calcs) - TB

What is this? (+upper lobe round nodules <1cm) - How to distinguish from talcosis? - What if calcs were central and smudgy? - What if lymph nodes with a low-attenuation center and peripheral rim enhancement

Right middle lobe, lateral segment (medial segment would abut the cardiac border)

What lobe and what segment?

Azygous vein (systemic vein)

What structure is this?

Right atrium: The right ventricle forms part of the anterior cardiac border on lateral chest radiography. The left ventricle and left atrium form the posterior cardiac border on lateral chest radiography. The right atrium is not border forming on the lateral chest radiograph.

Which cardiac chamber is not border forming on lateral chest radiography?

Left (in 97% of the time)

Which hilum is usually higher?