This document describes different types of lung cysts and cavities seen on imaging. It discusses the definitions, causes, and key radiologic features of pulmonary cysts, cavities, blebs, bullae, pneumatoceles, and other cystic lung lesions. Specific entities covered in detail include bronchogenic cysts, pulmonary sequestration, congenital cystic adenomatoid malformation, Langerhans cell histiocytosis, hydatid cysts, and cavitating tuberculosis. The document provides useful information to help distinguish these various cystic lung conditions based on appearance, characteristics, and associated clinical findings.

1. Presented by :
Passant Abdul Nasser Dorgham

3.  A cyst is a round space defined pathologically
by an epithelial or fibrous outer wall and
radiologically as a round parenchymal lucency
or low attenuation area with a well defined
interface with normal tissue.
 surrounded by a thin (2mm or less ) wall.
 A bleb or bulla has a wall that is less than 1
mm.

4.  Pulmonary cavities are gas-filled areas of the
lung in the center of a nodule, mass, or area of
consolidation.
 They are usually evident on plain radiography and
CT.
 They are typically thick walled and their walls
must be greater than 2-5 mm.
 They may be filled with air as well as fluid and
may also demonstrate air-fluid levels.

5. 1) Necrosis of lung parenchyma.
2) Communication with the tracheobronchial tree.
3) Complete destruction.
4) Band of inflammation around the necrotic
material.

6.  They include bronchiolar check-valve mechanism, vascular
occlusion or ischemia necrosis, and dilation of the
bronchioles.
 The valve mechanism in which the entrance from a
bronchus into a lung cavity become obstructed in a
valve-like manner, presumably with a piece of necrotic
tissue.
 Allows the ingress of air during inspiration but prevents
the egress during expiration.

8.  The cause of pulmonary cavities is broad.
 They may develop as a chronic complication of a
pulmonary cyst or secondary to cystic degeneration of
a pulmonary mass.
 They may enlarge or involute over time.

9. I. Cystic focal & multi-focal lung disease:
Cystic ( wall thickness less than 4 mm ).
Bullae .
Blebs.
Pneumatocele.
Congenital cystic lesions.
 Bronchogenic cyst.
 Congenital adenomatoid malformation.
Infections.
 Hydatid disease.
 Coccidioidomycosis.
 Pneumocystis carinii.
traumatic cysts.

10. II. Diffuse cystic lung disease:
 Pulmonary lymphangioleiomyomatosis.
 Pulmonary Langerhans cell histiocytosis.
 Honey comb lung.
 Idiopathic pulmonary fibrosis.
 Connective tissue disease ( related pulmonary
fibrosis).
 Asbestosis.
 Chronic hypersensitivity pneumonitis.
 Advanced sarcoidosis.
 Diffuse bronchiectasis.
 Metastatic disease ( rare).

11. III. Pediatric & developmental causes of lung cysts:
 Bronchogenic cysts.
 Pulmonary sequestration.
 Congenital cystic adenomatoid malformation.
 Lobar emphysema .
 Bronchial atresia .
 Lymphangiectasia.
 Pleuro-pulmonary blastoma.
IV. Non developmental causes:
 Pneumatocele.
V. others:
 Lymphatic cysts.
 Eneteric cysts.
 Mesothelial cysts.
 Simple arenchymal cysts.

12. I. cavitating malignancy:
 primary bronchogenic carcinoma (especially
squamous cell carcinoma)
 cavitating pulmonary metastases
 Adenocarcinoma
 sarcoma

13. II. non-infective granuloma
 granulomatosis with polyangitis.
 rheumatoid nodules.
III. vascular
 pulmonary infarct.
IV. trauma
 pneumatocoeles (a thin walled pneumatocoele is not
really a cavity).
V. congenital (not true "cavity")
 congenital cystic adenomatoid malformation (CCAM).
 pulmonary sequestration.
 bronchogenic cyst.

14.  a sub-pleural collection of air within the layers of
visceral pleura caused by a ruptured alveolus.
 The air dissects through the interstitial tissue into
the thin, fibrous layer of visceral pleura where it
accumulates to form a bleb.
 Rupture of a bleb is often associated with the
development of a spontaneous pneumothorax.
 It is usually less than 1 cm in diameter.

15.  An air filled space within the lung parenchyma
resulting from deterioration of the alveolar tissue.
 These lesions have a fibrous wall ,trabeculated by the
remnants of alveolar septa.
 Bullae can reach substantial size and occupy an entire
lobe
 Usually seen in chronic obstructive pulmonary disease
but also seen in normal young healthy individuals

18. Bulla results from destruction of alveolar walls (para-septal
emphysema).
The bleb results from rupture of alveolar air into the pleura .

19.  Pneumatocoeles are intrapulmonary air filled cystic
spaces that can have a variety of sizes and
appearances.
 They may contain air-fluid levels and are usually the
result of ventilator-inducted lung injury in neonates
or post-pneumonic.
 Associated with infection most commonly
staphylococcus aureus.
 It characteristically increases in size over a period of
days to weeks ( probably due to ball –valve air
trapping).

20. Radiographic findings:
 Smooth inner margins
 Contain air fluid level if any fluid
 Wall (if visible) is thin and regular
 Persist despite absence of symptoms

22. A) bronchogenic cyst.
 Bronchogenic cysts are numerous foregut buds
disconnected and separated from the tracheobronchial
tree to form a cystic mass during embryogenesis
(between 4th - 6th weeks).
 Most common site is middle mediastinum (65- 90%).
 Remote locations, including the interatrial septum,
neck, abdomen, and retroperitoneal space.

23. Clinical features:
 Most bronchogenic cysts are found
incidentally.
 In infants- compression of the trachea or
bronchi and esophagus-wheezing, stridor,
dyspnea, and dysphagia.
 Intra-parenchymal cysts may manifest with
recurrent infection.

25. Thin walled spherical unilocular masses –fluid filled, air filled or with
air fluid levels

27. Microscopically:
 Lined by secretory respiratory epithelium
(cuboid or columnar ciliated epithelium)
 Wall-cartilage, elastic tissues, mucous glands and
smooth muscle
 They do not usually communicate with the
bronchial tree, and are therefore typically not
air filled.
 Contain fluid (water), variable amounts of
proteinaceous material, blood products, and
calcium oxalate

29. B) Pulmonary sequestration:
 It is characterized by a portion of lung that
does not connect to the tracheobronchial tree
and has a systemic arterial supply, usually
from the thoracic or abdominal aorta.
 Two types of sequestration have been
described: intra lobar and extra lobar.
• The extra lobar form has its own pleural
investment and systemic venous drainage.
• The intralobar form shares the pleural
investment with the normal lung and
usually (but not invariably) drains into the
pulmonary venous system.

31. Clinical features:
 Intralobar sequestration
• Early childhood or adolescence with recurrence
lower lobe pneumonia
 Extra lobar
• Usually asymptomatic
• May have cyanosis and feeding difficulties
• Associated with diaphragmatic hernias, cardiac
malformations and foregut anomalies.

33.  Usually seen in the left lower lobe
 CT-homogenous soft tissue mass, cysts
containing air or fluid, focal emphysema or
hyper vascular focus of lung parenchyma
 Lung tissue is poorly developed and cystically
dilated
 Cysts lined by columnar to cuboidal epithelium

35. Gross pathology:
 Pleura thickened with adhesions
 Parenchyma-cysts up to 5cm with mucinous or purulent
material and fibrosis.

36. microscopically:
 Loose, spongy tissue with numerous small
cystic spaces containing clear, mucoid
fluid.
 Dilated bronchi with mucous or purulent
material
 Alveoli filled with foamy macrophages
 Thick walled vessels reflecting systemic
vascular drainage with elastic stains

38. c) Congenital cystic adenomatoid malformation (CCAM)
 multi-cystic mass of segmental lung tissue
with abnormal bronchial proliferation.
 It is considered part of the spectrum of
bronchopulmonary foregut malformations.
 They account for ~25% of congenital lung
lesions.
 there is a male predominance.

39. Pathogenesis:
 Failure of normal broncho-alveolar development
with hamartomatous proliferation of terminal
respiratory units in a gland-like pattern
(adenomatoid) without proper alveolar formation.
 These lesions have intra cystic communications
and, unlike bronchogenic cysts, can also have a
connection to the tracheobronchial tree.
 Lesions are usually unilateral and involve a single
lobe. Although there is no well-documented lobar
predilection, they appear less frequently in the
middle lobe.

40. Subtypes:
Five subtypes are currently classified, mainly according to
cyst size:
type I
o most common: 70% of cases 3
o large cysts
o one or more dominant cysts: 2-10 cm in size
o may be surrounded by smaller cysts
type II
o 15-20% of cases 3
o cysts are <2 cm in diameter
o associated with other abnormalities
o renal agenesis or dysgenesis
o pulmonary sequestration
o congenital cardiac anomalies

41. type III
o ~10% of cases
o micro cysts: <5 mm in diameter
o typically involves an entire lobe
o has a poorer prognosis
type IV
o unlined cyst
o typically affects a single lobe
o indistinguishable from type I on imaging 11
type 0
o very rare, lethal postnatally
o acinar dysgenesis or dysplasia 11
o represents global arrest of lung development 12

42. Radiographic features:
The appearance of CPAMs will vary depending on the type.
Antenatal ultrasound
o CPAM appears as an isolated cystic or solid intrathoracic mass.
o A solid thoracic mass is usually indicative of a type III CPAM
and is typically hyperechoic.
o There can be a mass effect where the heart may appear
displaced to the opposite side.
Plain radiograph
o Chest radiographs in type I and II CPAMs may demonstrate a
multicystic (air-filled) lesion.
o Large lesions may cause a mass effect with resultant mediastinal
shift, depression, and even inversion of the diaphragm.
o In the early neonatal period, the cysts may be completely or
partially fluid-filled, in which case the lesion may appear solid or
with air-fluid levels.
o Type III lesions appear solid.

43. CCAM type I
CT scan shows multiple large cysts (>2cm) involving the lower lobe of left lung. The cysts
are air-filled, expand the lower lobe, cause mediastinal shift and hypoplasia of right lung

44. CCAM type I

45. CCAM type I

46. a) pneumo cystitis carnii pneumonia :
 Cysts vary in size, shape, number, wall thickness
o Thin-walled (<3mm), usually air-filled
o Usually multiple, bilateral
o May be intraparenchymal or subpleural
o upper lobe predominance
 Cystic disease now occurs in 10-34% PCP cases
 Cysts in HIV patient are highly suggestive of PCP

47. Lung cysts are usually multiple, thin walled and bilateral, but range in size, shape and
distribution

48. Alveoli which are distended with honey- combed, foamy, brightly eosinophilic material .
There is a scanty inflammatory infiltrate composed
mainly of monocyte, occasional plasma cells and histiocytes.

49. b) Hydatid cysts:
 Hydatid cysts may be solitary or multiple, the number
depending mainly on the amount of ova ingested and
the number of embryos filtered through the liver and
lungs.
 A centrally located cyst is said to be usually round,
but may become oval or polycyclic. Inferior lobes most
commonly affected
 Intact: ruptured= 3:1

50. Calcified unilocular hydatid cyst. Contrast material enhanced
CT scan shows a round lesion with water attenuation and a ring like pattern of
calcification (arrows). This pattern represents calcification of the peri-cyst and
strongly suggests a diagnosis of hydatid cyst

51. Outer acellular laminated membrane, Germinal membrane& Protoscolices, attached and
budding from the membrane

52. c) Cavitating Pulmonary tuberculosis:
 Post-primary infections are far more likely to cavitate
than primary infections and are seen in 20-45% of
cases.
 In the vast majority of cases, they develop in the
posterior segments of the upper lobes (85%).
 The development of an air-fluid level implies
communication with the airway, and thus the
possibility of contagion.
 Endo-bronchial spread along nearby airways is a
relatively common finding, resulting in a relatively
well-defined 2-4 mm nodules or branching lesions
(tree-in-bud sign) on CT.

54. a) Pulmonary Langerhans cell histiocytosis:
 PLCH is typically a disease of young adults which
predominately affects the lungs and bones
 Very strong association with smoking(90%)
o interstitial lung disease.
o Lung affected in isolation or in association with organ
systems.
Pulmonary disease in PLCH is characterized by peri-
bronchiolar 1-10 mm nodules in the early stages
In later stages of PLCH, the major pulmonary finding
is cysts (present in 80% of patients) and there may
be no nodules present
Lung bases are relatively spared at all disease stages.

55. Characteristic combination of diffuse cysts and centrilobular micro-nodules

56. Gross pathology :
 Cysts more pronounced later
in the disease usually less
than 10mm in diameter may
measure up to 2 - 3
centimeters in size
 Thin-walled, but on occasion
may be up to a few
millimeters thick
 confluence of 2 or more
cysts results in bizarre
shapes :
o bilobed
o cloverleaf
o branching
o internal septations

57. Histopathology:
 The earliest histologic lesion of PLCH consists of proliferation of
Langerhans’ cells along small airways. These early cellular lesions
expand to form nodules 1 to 5 mm in diameter.
 The characteristic lesion is composed of variable numbers of
Langerhans’ cells,eosinophils,plasma cells, lymphocytes, fibroblasts,
and pigmented alveolar macrophages, which form a loosely
aggregated granulomas.
 These granulomas are typically centered around distal bronchioles,
where they infiltrate and destroy airway walls.
 As these cellular granulomas evolve, peripheral fibrosis forms
resulting in traction on the central bronchiole which becomes cyst-
like
 Evolution from nodule, through cavitating nodule and thick walled
cysts, to the 'stable‘ thin-walled cysts.

59. B) Bronchiectasis:
 Bronchiectasis, or the dilatation and distortion of bronchi and
bronchioles, may be mistaken for cystic airspace disease .
 Bronchiectasis may be the result of either a chronic suppurative
process or accompany lung fibrosis, when it is then referred to
as traction bronchiectasis.
 Cystic bronchiectasis can be differentiated from true cystic lung
disease by the continuous relationship of the cystic structure to
bronchial tree
 Approximately uniform, medium-sized cavities are typical of
cystic bronchiectasis.
 Valsalva and Mueller maneuvers produce rapid change in the size
of cysts, which freely communicate with the airways; this change
distinguishes cystic bronchiectasis from other conditions.

61. a)Squamous cell
carcinoma of the lung
 (SCC) is one of the non-small cell carcinomas of the
lung, overtaken by adenocarcinoma of the lung as the
most commonly encountered lung cancer.
 Squamous cell carcinoma accounts for ~30-35% of all
lung cancers and in most instances are due to heavy
smoking.
 Macroscopically these tumors tend to be off-white in
color, arising from, and extending into a bronchus.
 They invade the surrounding lung parenchyma and can
extend into the chest wall.
 Larger tumors have a tendency to undergo central
necrosis.

63. Radiographic features:
 The more central lesions may appear as a bulky hilum,
representing the tumor and local nodal involvement.
 Lobar collapse may be seen due to obstruction of a
bronchus.
 When the right upper lobe is collapsed and a hilar
mass is present, this is known as the Golden S sign.
 A more peripheral location may appear as a rounded
or speculated mass.
 Cavitation may be seen as an air-fluid level