DAVID SUTTON PICTURES ONLY FOR STUDY

1. 7 DIFFUSE LUNG DISEASE
DAVID SUTTON

2. DAVID SUTTON PICTURES
DR. Muhammad Bin Zulfiqar
PGR-FCPS III SIMS/SHL

3. • Fig. 7.1 Sarcoidosis. Bilateral hilar node
enlargement.

4. • Fig. 7.2 Sarcoidosis. There are multiple
mediastinal lymph nodes. S=superior vena
cava ; A =aorta.

5. • Fig. 7.3 Sarcoidosis. There is bilateral hilar lymph
node calcification. Some of the nodes are calcified
peripherally ('egg-shell' calcification). A pacing
electrode is present. Heart block is an occasional
complication of sarcoidosis.

6. • Fig. 7.4 Sarcoidosis.
HRCT scan through the
right lung shows
nodularity of the
bronchovascular
bundles due to multiple
sarcoid granulomas.
Nodules are also
evident in the
subpleural regions
adjacent to the chest
wall and major fissure
(arrows).

7. • Fig. 7.5 Sarcoidosis. Miliary, nodular opacities
are present throughout both lungs. One year
later the appearances were entirely normal.

8. • Fig. 7.6 Sarcoidosis. (A) Miliary nodules with areas of
coalescence peripherally. (B) After resolution of the
nodular shadowing there is mild mid and upper zone linear
scarring. (C) CT image through the mid zones in a different
patient demonstrating mild residual fibrotic change causing
mina[ traction bronchiectasis on the right. ????????

9. • Fig. 7.6 Sarcoidosis. (A) Miliary nodules with areas of
coalescence peripherally. (B) After resolution of the
nodular shadowing there is mild mid and upper zone linear
scarring. (C) CT image through the mid zones in a different
patient demonstrating mild residual fibrotic change causing
mina[ traction bronchiectasis on the right. ????????

10. • Fig. 7.7 HRCT scan at the level of the hila
showing conglomerate fibrotic masses with
radiation into the surrounding lung.

11. • Fig. 7.8 Sarcoidosis. Expiratory HRCT scan through
the lower zones There is air trapping as evidenced by
areas of parenchyma that remain lower attenuation
on expiration. Some of these correspond to
individual secondary pulmonary nodules.

12. • Fig. 7.9 Simple silicosis. Multiple, small
nodules are present throughout both lungs.

13. • Fig. 7.10 Simple silicosis. CT scan
demonstrates multiple well-defined
pulmonary nodules, most numerous in the
posterior lung parenchyma.

14. • 7.11 Progressive massive fibrosis (PMF).
Large confluent masses have formed.
Cavitation is evident on the left (arrow).

15. • Fig. 7.12 Early complicated silicosis. CT scan
demonstrates coalescence of nodules into
pulmonary masses.

16. • Fig. 7.13 Silicosis. (A) There is bilateral hilar
lymphadenopathy. Many of the nodes are calcified,
some of them peripherally. (B) Similar changes on CT.

17. • Fig. 7.14 Progressive massive fibrosis in a coal miner of 52.
(A) Nodular opacities are present throughout both lungs,
and several areas of more confluent shadowing are
present. (B) Four years later, lower zone masses have
migrated centrally, leaving peripheral areas of emphysema.
The upper lobe opacities have enlarged.

18. • Fig. 7.15 Male aged 54 with Caplan's
syndrome. Coal worker with rheumatoid
arthritis. Multiple rounded opacities are
present (some partly calcified).

19. • Fig. 7.16 Caplan's syndrome. There is a left-
sided cavitating pulmonary nodule (arrows)
on a background of pneumoconiosis.

20. • Fig. 7.17 Asbestosis. There is a fine subpleural
reticular infiltrate associated with low-volume
calcified pleural plaques (best seen in a left
paravertebral position).

21. • Fig. 7.18 Asbestos exposure of 25 years. Fine
reticulonodular shadowing in the mid and lower
zones is best seen on the right. Bullous disease is
present at the left base.

22. • Fig. 7.19 Asbestosis. (A) Chest radiograph
demonstrating loss of clarity of the cardiac silhouette
(shaggy heart). (B) HRCT reveals linear opacities and
also a carcinoma (on part B) adjacent to the right heart
border.

23. • Fig. 7.20 (A) Asbestos exposure has resuited in pleural
plaques. There are coarse parenchymal bands extending
arising from these plaques that are causing some
distortion of the lung architecture. (B) In a different patient
the result of asbestos exposure is the development of
diffuse pleural thickening. This predated the sternotomy.

24. • Fig. 7.21 HRCT demonstrating an extensive
subpleural linear stripe due to asbestosis.

25. • Fig. 7.22 Berylliosis. The patient had spent 35 years in
the glass-blowing industry making neon lights. The
chest radiograph shows diffuse reticular shadowing.
The appearance is indistinguishable from end-stage
sarcoidosis.

26. • Fig. 7.23 Farmer's lung. Patchy alveolar
opacification superimposed on a miliary
nodulation. The costophrenic angles are clear.

27. • Fig. 7.24 Extrinsic allergic alveolitis. (A) CT demonstrates
widespread patchy areas of increased attenuation
(ground-glass shadowing) representative of areas of
inflammatory infiltrate. (B) Similar appearances in a
different patient. Note the characteristic sparing of single,
or small clusters of, secondary pulmonary nodules.

28. • Fig. 7.25 Allergic alveolitis due to monoamine
oxidase inhibitor drug. The interstitial
shadowing was generalised throughout both
lungs. Complete resolution within 7 days.

29. • Fig. 7.26 Systemic lupus erythematosis.
Bilateral pleural effusions are present.

30. • Fig. 7.27 Rheumatoid disease. Two cavitating
necrobiotic nodules are visible in the right
lung.

31. • Fig. 7.28 Rheumatoid disease. Chest
radiograph (A) and HRCT (B) demonstrating
typical subpleural honeycomb changes of
pulmonary fibrosis. There is considerable
volume loss.

32. • Fig. 7.29 Systemic sclerosis. (A,B) The chest radiograph
demonstrates early fibrosis and dilatation of the
oesophagus, best appreciated on the lateral film (arrows).
(C) HRCT demonstrating fine basal fibrosis with some
honeycomb changes. The left diaphragm is elevated.

33. • Fig. 7.29 Systemic sclerosis. (A,B) The chest
radiograph demonstrates early fibrosis and
dilatation of the oesophagus, best appreciated on
the lateral film (arrows). (C) HRCT demonstrating
fine basal fibrosis with some honeycomb
changes. The left diaphragm is elevated.

34. • Fig. 7.30 Polymyositis. There is volume loss
due to basal fibrosis.

35. • Fig. 7.31 Ankylosing spondylitis. (A) Chest radiograph
demonstrating bilateral apical mycetoma (arrows). (B)
Ankylosing spondylitis in a different patient with
mycetoma formation confirmed on CT.

36. • Fig. 7.32 Wegener's granulomatosis. (A) There are several poorly
defined pulmonary masses, the largest in the left midzone
(arrows). (B) CT through the lung bases of a man with biopsy-
proven Wegener's. There are multiple mass-like lesions up to
several centimetres in size.

37. • Fig. 7.33 Bronchocentric granulomatosis.
There is a cavitating pulmonary mass.
Diagnosis was made following resection.

38. • Fig. 7.34 Simple pulmonary eosinophilia (Loffler's
syndrome). This patient had a marked transient blood
and pulmonary eosinophilia, with non-specific chest
symptoms. CT revealed patchy areas of ground-glass
density in both lung apices that cleared rapidly on
prednisolone therapy.

39. • Fig. 7.35 Chronic eosinophilic pneumonia.
Alveolar opacities distributed peripherally.
The vertical band in the right lung is
characteristic.

40. • Fig. 7.36 Chronic eosinophilic pneumonia in a
retired farmer. There is consolidation
paralleling the chest wall bilaterally.

41. • Fig. 7.37 Desquamative interstitial pneumonitis
(DIP). There is diffuse ground-glass change
throughout the lungs due to inflammatory
infiltrate. Note the relatively low density of the
larger bronchi and small bullae compared with
the remainder of the lungs.

42. • Fig. 7.38 Cryptogenic fibrosing alveolitis.
Miliary opacities and a little reticulation. The
apices are spared.

43. • Fig. 7.39 Cryptogenic fibrosing alveolitis. Ring
shadows are well seen in the right lower zone
due to coarse fibrosis and honeycomb formation.

44. • Fig. 7.40 Cryptogenic fibrosing alveolitis.
HRCT through the lung bases shows
subpleural fibrosis. Lung biopsy is likely to
reveal established fibrosis.

45. • Fig. 7.41 Cryptogenic fibrosing alveolitis. HRCT
shows a mixture of fibrosis and areas of ground-
glass change. Histological assessment of lung
biopsy will reveal a mixture of inflammation and
fibrosis. This patient may benefit from steroids
although the established fibrous component may
remain.

46. • Fig. 7.42 Histiocytosis. (A,B) Fine reticulonodular shadowing is
present throughout both lungs, producing a honeycomb pattern.
Note the line of biopsy staples (arrows). (C) CT demonstrates cystic
spaces and discrete nodules characteristic of histiocytosis.

47. • Fig. 7.42 Histiocytosis. (A,B) Fine reticulonodular shadowing
is present throughout both lungs, producing a honeycomb
pattern. Note the line of biopsy staples (arrows). (C) CT
demonstrates cystic spaces and discrete nodules
characteristic of histiocytosis.

48. • Fig. 7.43 Histiocytosis recurring following
transplantation. Note the sternotomy suture
wires.

49. • Fig. 7.44 Tuberous sclerosis. (A) There is a fine
reticular infiltrate . The right costophrenic angle is
blunted following pleurodesis. There is a loculated left
pneumothorax. (B) HRCT demonstrates multiple thin-
walled cystic spaces, and loculated pneumothorax.

50. • Fig. 7.46 Lymphangioleiomyomatosis. (A) Chest
radiograph demonstrating normal lung volumes
and multiple thin-walled cysts. (B) HRCT shows
normal lung between the discrete cystic spaces.

51. • Fig. 7.47 Neurofibromatosis. There are
multiple thin-walled cysts replacing the
normal lung parenchyma.

52. • Fig. 7.48 Pulmonary haemorrhage. Good
pasture's syndrome. Large alveolar opacities.

53. • Fig. 7.49 Acute
pulmonary
haemorrhage. There is
ground-glass change in
the posterior aspect of
the right lung, due to
alveolar haemorrhage.
Note the generalised
nodularity due to the
effects of recent
haemorrhage.

54. • Fig. 7.50 Pulmonary haemosiderosis, chronic
phase. There is diffuse ill defined nodular
change, mainly in the posterior aspect of the
lungs.

55. • Fig. 7.51 Mitral stenosis with pulmonary
ossification due to haemosiderosis.

56. • Fig. 7.52 ARDS reaction to methotrexate
administration. Note the anterior posterior
gradient of increase in lung density.

57. • Fig. 7.53 (A) Amiodarone toxicity. There are enlarged
mediastinal lymph nodes (curved arrows). Note the
area of dense peripheral consolidation due to
amiodarone deposition (arrow). (B) Same patient on
lung windows demonstrating coarse fibrosis. (C) Lung
fibrosis in a different patient on long-term pizotifen
therapy.

58. • Fig. 7.53 (A) Amiodarone toxicity. There are enlarged
mediastinal lymph nodes (curved arrows). Note the area of
dense peripheral consolidation due to amiodarone
deposition (arrow). (B) Same patient on lung windows
demonstrating coarse fibrosis. (C) Lung fibrosis in a
different patient on long-term pizotifen therapy.

59. • Fig. 7.54 Pulmonary talcosis due to repeated
injection of ground-up tablets. There is diffuse
increase in attenuation of the lung compared
with the trachea.

60. • Fig. 7.55 Pulmonary talcosis. (A) There are perihilar
masses with radiating strands of fibrosis distorting the
surrounding pulmonary architecture. Compare with
Fig. 7.7. (B) CT scan on mediastinal window setting in a
different patient demonstrating high attenuation in the
perihilar masses.

61. • Fig. 7.56 Amyloidosis. CT scan reveals
multiple small pulmonary nodules scattered
through the lungs. In this patient these were
non-calcified.

62. • Fig. 7. 57 (A) Pulmonary alveolar proteinosis.
Central alveolar patchy densities and vague
nodulation. (B) Close-up. ill-defined alveolar
opacities; air bronchogram visible.

63. • Fig. 7.58 Alveolar proteinosis. Typical crazy-
paving appearances with alveolar filling and
septal wall thickening.

64. • Fig. 7.59 (A) Pulmonary alveolar microlithiasis. Multiple, fine,
dense opacities are visible throughout the lungs. HRCT on lung
(B) and mediastinal (C) window settings. Innumerable tiny nodules
are present, and there is a marked subpleural lucent line that may
be apparent on scrutiny of the chest radiograph. The high-density
nature of the lesions is apparent adjacent to the mediastinum.

65. • Fig. 7.59 (A) Pulmonary alveolar microlithiasis. Multiple,
fine, dense opacities are visible throughout the lungs.
HRCT on lung (B) and mediastinal (C) window settings.
Innumerable tiny nodules are present, and there is a
marked subpleural lucent line that may be apparent on
scrutiny of the chest radiograph. The high-density nature of
the lesions is apparent adjacent to the mediastinum.