Radiological and Clinical features of diffuse lung diseases. Especially, HRCT features and some pathognomonic findings of diffuse lung disease. Cystic lung diseases, Nodular lung diseases, Fibrotic lung diseases, Smoking related lung diseases,

1. Radiological Approach
To
Diffuse Lung Diseases
Dr. Soe Moe Htoo

3. Practical approach to diffuse lung diseases
1. Analysis of “distribution” of the abnormalities,
2. Interpretation of “pattern” in relation to distribution,
3. Utilization of associated imaging findings and clinical information, and
4. Chronicity of the findings.

4. Distribution of Abnormalities
Distribution is classified as follows:
1) upper, middle, lower lung distribution;
2) peripheral or central; and
3) distributions relation to a secondary pulmonary lobule
i. lymphatic,
ii. centrilobular, and
iii. random

5. 2-1. Upper, middle and lower lung distribution,
Dividing lungs into three areas (in cranio-caudal direction)
Upper lung Predilection  sarcoidosis, hypersensitivity
pneumonitis, silicosis
Lower Lung Predilection  idiopathic pulmonary fibrosis (IPF),
non-specific interstitial pneumonia (NSIP)

6. 2-2. Peripheral or central distribution
Peripheral lung :
consists of two or three rows of secondary pulmonary lobules
forming a layer of three to four centimeter in thickness at the lung
periphery and along the lung surfaces adjacent to fissures
Peripheral distribution  cryptogenic organizing pneumonia, IPF,
NSIP)
Central lung  remaining lung
Central distribution  cardiogenic pulmonary edema or alveolar
proteinosis

7. 2-3. Secondary pulmonary lobule
•Fundamental unit of lung structure
•Key to understanding the distribution of diffuse lung disease
•Polygonal shaped structure composed of several acini conducted
by terminal bronchiole
•Number of acini in the secondary lobule is variable (ranging from
3 to over 20)
•Size 1-3 cm

8. •Interlobular septum defines the boundary of the secondary
pulmonary lobule.
•The bronchus and artery (bronchovascular bundle) run into the
center of the secondary pulmonary lobule (Fig. 3B)
•Analysis of which component of the secondary pulmonary lobule
is involved is the key step to determine the distribution of the
diffuse lung disease

9. Lymphatic distribution
Pulmonary lymphatic system exists both along the
bronchovascular bundle and interlobular septum.
Major differential diagnoses
1) pulmonary oedema,
2) sarcoidosis,
3) lymphangitic spread of tumour or lymphoma (Table 1).

10. Centrilobular distribution
•Small airway related diseases
•Predominantly bronchovascular bundle involvement (Fig. 5)
•Hallmark of the centrilobular distribution:
sparing of interlobular septa (unless the disease process
completely fills the whole secondary pulmonary lobule)

11. Random distribution
No relation to secondary pulmonary lobule
Major differential diagnoses
1) Miliary tuberculosis
2) Hematogenous metastasis
3) Disseminated fungal infection

12. Could this be UIP or NSIP?
•UIP and NSIP are the two most common forms of idiopathic
interstitial lung disease.
•On HRCT, UIP and NSIP show peripheral and basilar distribution
often with decreased lung volumes.
•Honeycombing is common in UIP and is uncommon in NSIP.
•Clinical outcome and prognosis is substantially better in NSIP
than in UIP

13. 3-1. Usual interstitial pneumonia (UIP)
•UIP is a histologic diagnosis and represents a lung reaction
pattern to injury
Causes
1) Idiopathic (called idiopathic pulmonary fibrosis)
2) Secondary to exposure to dusts (e.g., asbestos)
3) Drugs (e.g., bleomycin)
4) Collagen vascular diseases

14. •Heterogeneous appearance with alternating areas of:
i. Normal lung
ii. Interstitial inflammation
iii. Fibrosis
iv. Honeycomb change
•Interstitium - scattered clusters of fibroblasts and immature
connective tissue (fibroblastic focus)

15. Characteristic HRCT features of UIP:
1) Peripheral and basilar distribution
2) Interlobular septal thickening
3) Ground glass opacities
4) Honeycombing
5) Traction bronchiectasis
6) Decreased lung volume unless associated with emphysema
(Fig. 6).

16. Honeycombing
•Clustered cystic air spaces (average size 0.3–1 cm)
•Lined by bronchiolar epithelium and dense fibrous tissue (1–3 mm
thick walls)
•Indicates end-stage fibrotic lung disease
•Predominantly peripheral and subpleural distribution (Fig. 6).

17. Idiopathic Pulmonary Fibrosis (IPF)
•Progressive fibrosis, End-stage lung destruction, Unknown cause
•Morphologic pattern of UIP
•Careful clinical evaluation to exclude an underlying aetiology
(Need to be idiopathic)

18. Clinical Features
1) Progressive shortness of breath, Wt. loss, Clubbing
2) Non-productive cough (usually more than 6 months)
3) Age - over 50 years
4) Men slightly more affected
5) Not respond to steroid treatment
6) Poor prognosis (median survival < 5 years)
Complications of IPF
1) Accelerated progression
2) Lung cancer
3) Secondary infection

19. CXR
•B/L asymmetrical peripheral reticular opacities
•Predominantly at lung bases
•Lung volume - reduced or preserved (association with
emphysema)

20. HRCT
•Disease progress  also involve anterior aspects of upper lobes
•Mediastinal lymphadenopathy up to 2 cm (unrelated to infection and
malignancy)
•Early stage : GGO
•Late stage : subpleural bibasal reticular pattern
•End stage : areas of honeycomb destruction with associated traction
bronchiectasis

21. Nonspecific Interstitial Pneumonia (NSIP)
•Histology - inflammation and fibrosis predominantly involving the
alveolar walls
•Idiopathic or in relation to collagen vascular diseases,
hypersensitivity pneumonitis, and drug-induced lung disease.
•Temporal and spatial homogeneity (key feature of NSIP)
•Clinical symptoms  similar UIP, usually milder.
•NSIP has more favourable prognosis than UIP
•Male=Female, Mean Age - 40 years

22. •Two subtypes:
1) Cellular (lung inflammation predominate)
2) Fibrotic (fibrosis predominate)
•Prognosis is poorer in fibrotic NSIP

23. Predominant ground glass opacity in NSIP
More likely to respond to steroid treatment
Parenchymal abnormalities (traction bronchiectasis and
ground-glass opacity) may be reversible at follow up

24. Characteristic HRCT features of NSIP
(Overlap in radiographic appearance between NSIP and UIP)
•Basal and subpleural predominant ground glass opacities
•Traction bronchiectasis
•Lower lobe volume loss
•No or mild honeycombing (Fig. 8)

25. Interpretation of “Pattern” in relation to
“Distribution”
1. Diseases of the lymphatic system
1) Pulmonary Oedema
2) Sarcoidosis
3) Lymphangitis spread of tumour or lymphoma
2. Nodular lung diseases
1) Random
2) Centrilobular
3) Lymphatic distribution (Interstitial)

26. Diseases of the lymphatic system
•Involve interlobular septum, fissure, pleura and along the
bronchovascular bundles
•Demonstrate thickening of these structures
•Septal and bronchovascular bundle thickening can be smooth,
irregular, or beaded, depending of the diseases.
•Major differential diagnoses
1) pulmonary oedema,
2) sarcoidosis,
3) lymphangitic spread of tumour or lymphoma (Table 1).

27. Pulmonary oedema
•Most common among the diseases of the lymphatic system
•Smooth interlobular septal thickening (Fig. 10).
•Associated imaging findings:
1) Diffuse ground glass opacities
2) Pleural effusion
3) Cardiomegaly
•Clinical information is important.

28. Sarcoidosis
•Multisystem, Non-caseating, Granulomatous disorder, Unknown
aetiology
•Most affected : lungs, hilar and mediastinal nodes
•Other : skin > peripheral nodes > eyes > spleen > CNS > parotid
gland > bones
•2nd-4th decade, F > M

29. Radiological Features
•Usually upper and middle lung distribution
•Beaded or irregular appearance with a thickened bronchovascular
bundle, interlobular septum, fissure and pleura (d/t granulomatous
infiltration along lymphatics) (Fig. 11)
• CXR Staging
1) Stage 0 : Normal CXR
2) Stage 1 : Lymphadenopathy
3) Stage 2 : Lymphadenopathy + Parenchymal opacification
4) Stage 3 : Parenchymal opacification only
5) Stage 4 : Pulmonary fibrosis

30. •Lymph node
1) Bilateral symmetrical lobulated, well demarcated outline
2) +/- Egg-shell calcification (DD: BLASH)
3) Garland’s triad (B/L symmetrical hilar and paratracheal
lymphadenopathy
4) + nodal enlargement  40% develop parenchymal opacities
within 1 year (II)  1/3 progress to pulmonary fibrosis (IV)
5) Nodal enlargement does not develop after parenchymal
opacification

31. •Rounded or moderately well-defined peri-lymphatic nodules (2-4
mm) within subpleural, along bronchovascular bundles and
interlobular septae
•Peri-bronchovascular patchy air-space consolidation (can
demonstrate air bronchogram)
•Patchy GGO
•Associated imaging findings
1) symmetric and bilateral mediastinal and hilar lymphadenopathy
2) architectural distortion due to chronic inflammation
3) extensive fibrosis in upper lung distribution with volume loss

32. •Associated clinical features
1) Uveitis
2) Elevated angiotensin-converting enzyme level
3) Sarcoidosis in other organ systems

33. Lymphangitic spread of the tumour and lymphoma
•Typically lower lung distribution (Fig. 12).
•Can be asymmetric
Associated imaging findings
1) Lymphadenopathy in the mediastinum, axilla, supraclavicular
areas and upper abdomen (can be asymmetric or necrotic)
2) May present primary tumour
3) Architectural distortion and extensive fibrosis are not usually
present. (Cf. Sarcoidosis)

34. Nodular lung disease
1. Random nodules
The hallmark of this useful pattern is random distribution of
nodules in relation to the secondary pulmonary nodule.
•Nodular pattern can be further classified according to nodule size:
(1)“fine” nodules (approximately 3 mm or less)
(2)“medium or large” sized nodules (> 3mm)

35. Differential diagnosis for “fine” nodules with random distribution is
1) miliary tuberculosis
2) Metastasis
3) disseminated fungal infection (Fig. 13).
Differential diagnosis for “medium or large” sized nodules with random
distribution
1) Metastasis,
2) Metastasis, and
3) Metastasis
In immunocompromised hosts, fungal infections or tuberculosis can present
with nodules that are larger than fine nodules (Fig. 14) (Table 1).

36. 2. Centrilobular nodules
•Seen along the bronchovascular bundle (Fig 3B),
•Disease process is along the airway
•Most likely due to infection or inflammation
•Nodules can be discrete or ill-defined (Fig. 15).
•To confirm absence of interlobular septal thickening to
differentiate centrilobular nodules from diseases of lymphatic
system. (Critical)

37. •Aetiology of the centrilobular nodules is usually benign
(except for neoplasm spreading along the airway such as
bronchoalveolar carcinoma or lymphoma) (Table 1).
•Diagnosis can be reached via bronchoscopy for most of diseases
with centrilobular nodules.

38. Sometimes associated with branching opacities or “tree-in-bud”
opacities  dilated centrilobular bronchioles impacted with mucus,
fluid or pus
1) endobronchial spread of tuberculosis or atypical mycobacterial
infection
2) infectious bronchiolitis and
3) diffuse panbronchiolitis (Fig. 16)

39. 3. Nodules in lymphatic distribution
•Diseases of the lymphatic system, especially sarcoidosis, should
be considered (Fig. 11) (Table 1).
•Lymphatic spread of the tumour or lymphoma may demonstrate
nodules in lymphatic distribution.

40. Ground-glass opacity
•Non-specific term
•Presence of a hazy increase in lung opacity without obscuration of
underlying vessels
•GGO has long list of differential diagnoses, almost anything
occupying either alveoli or interstitium, or both.
•Associated clinical information is crucial in interpretation of cases
with ground-glass opacities.

41. Differential diagnoses of GGO
1) Hypersensitivity pneumonitis,
2) Pneumocystis jirovecii pneumonia (PCP)
3) Cytomegalovirus (CMV) pneumonia,
4) Pulmonary oedema
5) Adult respiratory distress syndrome (ARDS)
6) Diffuse pulmonary haemorrhage

42. •Analysis of distribution sometimes helps in differential diagnosis
of ground-glass opacity.
•Peripheral GGO
1) NSIP
2) COP
3) DIP
•Centrilobular GGO
1) hypersensitivity pneumonitis
2) RB-ILD.
•Central GGO
1) Pulmonary oedema (if acute)
2) Alveolar proteinosis (if chronic)

43. Hypersensitivity Pneumonitis
•Allergic lung disease
•Results from inhalation of a variety of organic dust antigens
•Histology: interstitial mononuclear cell infiltrate, cellular
bronchiolitis and non-necrotizing epithelioid granulomas.
•Clinical information regarding exposure history to a certain
antigen is useful when interpreting HRCT.
•GGO + Air-trapping, upper & mid zone  hypersensitivity
pneumonitis

44. Classified into three types;
1. Acute disease (symptoms lasting < 1 month)
•Limited HRCT findings, can be normal during acute episode
•Diffuse GGO +/- alveolar consolidation esp. lower zone
2. Subacute disease (over weeks to 4 months/ episodic flare up)
•Poorly defined centrilobular nodules (< 5 mm), mid and lower zone
•GGO
•Mosaic attenuation - lobular areas of decreased vascularity with Air
trapping on expiratory HRCT (Fig. 17).
3. Chronic disease ( 4 months  several years)
•Mid and upper lung fibrosis, sparing costophrenic angles
•Reduced lung volume, honey combing, traction bronchiactasis
•Pulmonary arterial hypertension

45. PCP and CMV Pneumonia
•Important differential diagnosis for ground-glass opacity
•Especially immunocompromised patients with infectious symptom
(Fig. 18).
•PCP is a common life-threatening opportunistic infection in AIDS
patients with CD4 counts of less than 200 cells/mm3

46. Pulmonary oedema
•One of the most common diffuse lung diseases with GGO
•HRCT demonstrates ground-glass opacity in central distribution
(Fig.19)
•often associated with smooth interlobular septal thickening.

47. ARDS
•Diffuse lung injury  permeability oedema and diffuse alveolar
damage.
•HRCT: diffuse or patchy GGO or consolidation, predominantly in
dependent lung regions.
•The patients are often intubated because of severe respiratory
distress.
•Clinically, ARDS is characterized by dyspnoea and hypoxemia
which develop over hours or days.
•The time course of the development and changes in the opacities
should be carefully correlated with onset and changes in clinical
symptoms.

48. Diffuse pulmonary haemorrhage
•Patchy or diffuse ground-glass opacity
•Consolidation or ill-defined centrilobular opacities (Fig. 20).
Causes of pulmonary haemorrhage
1) antiglomerular basement membrane disease (Goodpasture’s syndrome),
2) vasculitis such as Wegener’s granulomatosis and Churg-Strauss
syndrome
3) collagen vascular diseases such as systemic lupus erythematosus,
4) idiopathic pulmonary hemosiderosis,
5) intrinsic or extrinsic coagulopathy, and
6) drug reaction

49. •Specific diagnosis regarding the cause of hemorrhage is usually
difficult on HRCT findings, and clinical information about the
underlying diseases is necessary for further differentiation among
these diseases.

50. Pulmonary alveolar proteinosis
•Filling of the alveolar spaces with a periodic acid-Schiff-positive lipid-rich
proteinaceous material
•Most common age 30 - 50 years
•Symptoms are usually mild and of insidious onset
•Non-productive cough, fever, and mild dyspnoea
•HRCT findings include bilateral GGO in patchy or geographic distribution
associated with smooth interlobular septal thickening (crazy-paving)

51. 5. Advanced Problems
•The basic approach described above will cover most of the diffuse lung
disease cases
encountered in daily clinical practice.
•However, there are still some disease categories that remain to be
described.
•In this section, we will discuss advanced problems including smoking-
related diffuse lung diseases, diffuse lung disease with increased lung
volume, and bilateral multiple parenchymal opacities (Table 2).

52. 5-1. Smoking-related diffuse lung diseases
1) Respiratory bronchiolitis-associated interstitial lung
Disease (RB-ILD)
2) Desquamative interstitial pneumonia (DIP)
3) Langerhans cell histiocytosis (LCH)

53. RB-ILD
•symptomatic interstitial lung disease associated with pathologic
lesions of respiratory bronchiolitis
•On histology, bronchiolocentric accumulation of pigmented
alveolar macrophages with mild bronchiolar fibrosis and chronic
inflammation

54. HRCT features:
1) Centrilobular ground-glass opacities
2) Thickening of central and peripheral airways
3) Associated centrilobular emphysema and air trapping
4) Predominantly affects upper lobes

55. DIP
•idiopathic interstitial pneumonia associated with cigarette smoking
•characterized by the presence of increased numbers of pigmented macrophages
evenly dispersed within alveolar spaces
Clinically,
•Both RB-ILD and DIP affect cigarette smokers 30–40 years of age (M:F - 2:1)
•Pulmonary function tests demonstrate a restrictive abnormality and decreased
DLCO.
•Significant overlap between RB-ILD and DIP is seen in clinical, radiological and
pathological findings
•Reflect different degrees of severity of the small airways and parenchymal reaction
to cigarette smoking
•DIP being the end spectrum of RB-ILD

56. HRCT findings:
•Ground-glass opacity
•Distribution: Peripheral-patchy or diffuse-uniform with interlobular
septal thickening (Fig. 21).
•Predominantly lower lung distribution

57. Pulmonary LCH
•Uncommon diffuse lung disease
•Histologically : destruction of distal airways by bronchocentric granulomas
containing Langerhans cells (large histiocytes)
•The etiology is unknown; however, LCH typically associated with cigarette
smoking
Clinically,
•equally affects men and women,
•Associated with smoking history.
•Prognosis varies from complete remission after smoking cessation to
development of cystic lung disease.

58. HRCT findings
1) Bilateral symmetrical widespread involvement
2) Cysts and nodules with centrilobular distribution
3) Upper and middle lung predominance
4) Sparing of extreme lung bases (costophrenic angles, anterior
tips of middle and lingular lobes)
5) Lung volumes - normal or increased

59. Cyst
•Size - usually less than 1 cm in size; however, can be larger (≥2–3
cm), not uniform in size
•Shape - round but sometimes confluent or bizarre
•Walls - thin (hair-line) but can be as thick as several millimetres
Nodules
•Size - varying sizes (1–5 mm, 5–10 mm, or larger) with indistinct
margins
•Cavitation of the nodule is often seen (relatively thick wall)

60. Diffuse lung disease with increased lung
volumes
1. Lymphangioleiomyomatosis (LAM)
2. Pulmonary LCH
3. Emphysema with fibrosis

61. Lymphangioleiomyomatosis (LAM)
•Rare, idiopathic disorder of the lung parenchyma
•Non-neoplastic proliferation of smooth muscle cells of bronchioles, pulmonary
vessels and lymphatics
•Almost exclusively females of child-bearing age (20-40 years)
•Symptoms include dyspnea on exertion, and sometimes with pneumothorax,
leading to progressive loss of pulmonary function.
•Clinical course is usually slowly progressive, leading to respiratory failure and
death.
•Treatments - antiestrogen therapy & lung transplantation
•In contrast to LCH, LAM has no definite relation to smoking.

62. High-resolution CT findings
1) Bilateral symmetrical widespread involvement (no zonal
predilection, more diffuse and random distribution involving the
costophrenic angles)
2) Multiple more regular shaped thin-walled cysts and relatively
uniform in size
3) Ground glass opacities
4) Mild septal thickening
5) Increased lung volumes
6) Association with recurrent pneumothorax (50% of patient) and
pleural effusion (10-40%)

63. •Differentiation between pulmonary LCH and LAM is often possible
using clinicopathological and radiological features.
•Combination of cysts and nodules  LCH
•Multiple thin-walled cysts with diffuse random distribution  LAM
•Costophrenic angle involvement  LAM

64. Emphysema with fibrosis
•Relatively common and frequently encountered.
•Emphysema predominantly distributes centrally in upper and
middle lung areas
•Fibrosis predominantly distributes peripherally in lower lung area
and base
•Combination of obstructive changes from emphysema and
restrictive changes from fibrosis may demonstrate normal
pulmonary function, which can be misleading.
•Awareness of this combination and evaluation on HRCT is
important.

65. 5-3. Bilateral Multiple Parenchymal Opacities
•seen as multiple areas of increased lung attenuation, and are usually less
round than nodules
•possibly represent infection, neoplasm, or vasculitis or other inflammatory
pathology.
•In the interpretation of bilateral multiple parenchymal opacities, the analysis
of distribution is important.
•Peripheral distribution in organizing pneumonia (COP), chronic eosinophilic
pneumonia (CEP), and thromboembolic diseases

66. •In clinical practice, infection and neoplasm must be considered
first.
•If they are not likely based on clinical correlations, interstitial lung
disease and vasculitis should be considered next.
•Thromboembolic disease is a pitfall that should be kept in mind.

67. Infection
•Bilateral multifocal parenchymal opacities can be seen in a variety
of infectious processes, including bacterial or fungal infection.
•Among them, clinically important etiologies to be recognized
include invasive aspergillosis, cryptococcosis, coccidioidomycosis,
and nocardiasis.
•These organisms most typically affect immunocompromised
patients.

68. Invasive aspergillosis
•Involvement of normal lung tissue by Aspergillus organisms
HRCT findings:
•Early phase - ill-defined nodular or consolidative opacities with
surrounding ground glass opacities (halo sign) (Fig. 24)
•Late phase - Cavitary nodules with air-crescent due to necrosis

69. Neoplasm
•Bilateral multifocal parenchymal opacities causing neoplasm 
bronchioalveolar cell carcinoma, lymphoma and lymphoproliferative
disorders.
•HRCT appearance can be indistinguishable from pneumonia
•Correlation with clinical symptoms and observation of chronicity and
chronological changes of the finding by comparing prior studies are
necessary.

70. Cryptogenic Organizing Pneumonia, Chronic
Eosinophilic Pneumonia, and Vasculitis
•Most cases of bilateral multiple parenchymal opacities presenting
with fever and shortness of breath are thought to be caused by
infectious processes and treated as such.
•However, in some cases, such treatment fails, typical infectious
process less likely.
•In these instances, atypical infection especially fungal infection
and next category of diseases, including cryptogenic organizing
pneumonia (COP), chronic eosinophilic pneumonia (CEP) and
vasculitis should be considered

71. COP
•Formerly called bronchiolitis obliterans organizing pneumonia (BOOP)
•Organizing pneumonia of idiopathic cause
Clinical Symptoms
•Cough, dyspnoea, malaise, fever, and weight loss
•COP resolves spontaneously, but often needs steroid treatment
On Histology
•Presence of granulation tissue filling the bronchiolar lumen and alveolar
ducts.
•Chronic inflammation and interstitial fibrosis of alveolar walls can be seen.
•The overall histologic feature has temporal homogeneity

72. On HRCT
•Patchy bilateral parenchymal consolidation with peripheral and
lower lung distribution
•Associated ground-glass opacities (Fig. 26)

73. CEP
•Idiopathic
•Characterized by eosinophil-rich exudates in alveoli and
interstitium on histology
Clinically,
•history of allergic diseases (atopic dermatitis, asthma, rhinitis,
sinusitis, etc.).
•Cough with mucoid sputum, high fever and night sweats (severe
and usually last more than 3 months)

74. CXR
•Peripheral, non-segmental homogeneous consolidation with or
without air-bronchogram, so-called “photographic negative of
pulmonary oedema”
HRCT features:
•Patchy parenchymal consolidation with peripheral and upper lung
distribution
•Associated ground-glass opacities
•Linear or band-like subpleural opacities

75. •As both COP and CEP have multiple consolidative opacities in
peripheral distribution, the differentiation between the two entities
can be difficult.
•Clinical information is important to further differentiate the entities.

76. Vasculitis
•includes a large and varied group of disorders
•characterized by inflammation and necrosis of blood vessels
•Frequency and manifestation of lung involvement in vasculitis vary greatly.
Typical Presentations of Pulmonary Vasculitides
•Bilateral multifocal parenchymal opacities
•Diffuse pulmonary haemorrhage

77. Wegener’s granulomatosis
•Characterized by necrotizing granulomatous vasculitis of the respiratory tract,
segmental glomerulonephritis and small vessel vasculitis
•Approximately 90% of patients have lung involvement.
Symptoms:
•sinusitis, cough, hemoptysis, or hematuria.
•More than 90% of patients have a positive cytoplasmic antineutrophil
cytoplasmic antibody (cANCA)

78. HRCT findings:
•Bilateral, multiple, rounded opacities with varying size in random
distribution (Fig. 27).
•Cavitation is common, with a thick wall and irregular inner lining.
•Consolidation and ground glass opacities are often associated
with pulmonary haemorrhage

79. Allergic angiitis and granulomatosis (Churg-
Strauss syndrome)
•Characterized by necrotizing vasculitis, extravascular granuloma formation, and
eosinophilic infiltration.
•It is a multisystem disorder with predilection for the lungs, skin, nervous system,
gastrointestinal tract, heart, kidney and joints.
HRCT findings:
•Air-space consolidation or ground glass opacities in a peripheral distribution,
•Multiple nodular lesions of varying size
•Cavitation of nodules is less common compared to Wegener’s granulomatosis
•Allergic diseases including asthma, nasal polyps and sinusitis are often present, and
therefore, clinical history about these co-existent diseases should be examined.

80. Thromboembolic diseases
•It is a pitfall of differential diagnosis in multiple parenchymal
opacities.
•Rare, patients with thromboembolism presenting with multiple
parenchymal opacities on chest radiograph or CT
•can be misinterpreted to have any of the diffuse lung diseases
described above.
•Therefore, it is important to consider possibility of thromboembolic
diseases in differential diagnosis in multiple parenchymal
opacities.

81. Pulmonary embolism with infarction
•Pleura-based or wedge-shaped opacities with increased attenuation and
peripheral distribution are demonstrated on CT.
•These opacities do not show enhancement by intravenous contrast agent (if
administered), representing pulmonary infarction
•In pulmonary embolism without infarction, multiple parenchymal opacities
are also seen, commonly with lower lung distribution, representing
atelectasis.
•When these findings are present, they should be correlated with clinical
information including symptoms such as dyspnea, pleuritic chest pain,
tachypnea, and tachycardia, D-dimer assay, and the presence/absence of
deep venous thrombosis.
•When pulmonary embolism is suspected, pulmonary CT angiography should
be performed to directly visualize emboli

82. Septic embolism
•Occurs when fragments of thrombus include micro-organism (most commonly
bacteria)
CT
•multiple parenchymal opacities,
•Discrete nodules with varying degrees of cavitation
•Subpleural, wedge-shaped opacities, predominantly in the lower lobes (Fig. 28)
Common predisposing factors
•tricuspid valve endocarditis with or without drug addiction
•alcoholism,
•skin infection
•immunologic deficiencies (particularly lymphoma)
•Infected venous catheters or pacemaker wires

83. Pitfall
•The presence of underlying emphysema can modify the appearances of
common conditions and make them look like unusual presentations of diffuse
lung disease.
•Of particular importance is emphysema with pneumonia, for this condition
requires that the patient receive immediate treatment by antibiotics.

84. Conclusion
•High-resolution CT of diffuse lung diseases provides broad differential
diagnosis as well as diagnostic challenges.
•The practical approach described in this article focuses on the importance of
distribution of the abnormalities and interpretation of pattern in relation to
distribution.
•This approach is designed to provide a practical solution for radiologists who
are facing the increasing necessity of interpreting HRCT with advances in
multidetector row CT technology.

85. NSIP VS UIP
NSIP
• Prominent GGO
• Fine reticular pattern
• Absence of honeycombing
• Better prognosis than UIP
LAM VS LCH
LAM
• Female
• Not associated with smoking
• More diffuse distribution (no
sparing of lung bases)
• More regular shaped cysts
• Cysts + Nodule  LCH
• Cysts only  LAM