Describes the basic radiology of diffuse interstitial disease ,with differential diagnosis of reticular interstitial pattern and how to approach HRCT findings .

1. HRCT
Reticular pattern
DR SAKHER-ALKHADERI
CONSULTANT RADIOLOGIST AMC

2. INTRODUCTIONINTRODUCTION
• HRCT -- Use of thin section CT images (0.625 to 2
mm slice thickness) often with a high-spatial-
frequency reconstruction algorithm to detect and
characterize disease affecting the pulmonary
parenchyma and airways.
• Superior to chest radiography for detection of lung
disease, points a specific diagnosis and helps in
identification of reversible disease.
2

3. 3

4. Thin section produces better contrast
between lung parenchyma and
bronchus and pulmonary vessel. A scan
obtained with increased slice thickness,
produces volume averaging with
blurring of pathological details.

5. The division of trachea gives rise to the
left and right mainstream bronchi, which
further divides into lobar and segmental
bronchi. Segmental bronchi divides
after 6 to 20 division they no longer
contain cartilage in their walls and are
referred to as bronchioles.

6. There are approximately 23
generation of dichotomous
branching
From trachea to the
alveolar sac
HRCT can identify upto 8th
order central bronchioles
6

8. SUBJECTS
Anatomy of the secondary lobule
Basic HRCT patterns
Distribution of abnormalities
Differential diagnosis of interstitial lung
diseases

9. Secondary lobule
• The secondary lobule is the basic anatomic
unit of pulmonary structure and function.
Interpretation of interstitial lung diseases is
based on the type of involvement of the
secondary lobule.
It is the smallest lung unit that is surrounded
by connective tissue septa.
It measures about 1-2 cm and is made up of
5-15 pulmonary acini, that contain the alveoli
for gas exchange.

10. Secondary lobule
Basic anatomic unit of pulmonary
structure and function.
1-2 cm and is made up of 5-15
pulmonary acini
Supplied by a small bronchiole
(terminal bronchiole) in the
center, that is parallelled by the
centrilobular artery.
Pulmonary veins and lymphatics
run in the periphery
Two lymphatic systems:
 central network
 peripheral network

11. Secondary lobule

12. • The secondary lobule is supplied by a
small bronchiole (terminal bronchiole) in
the center, that is parallelled by the
centrilobular artery.
Pulmonary veins and lymphatics run in the
periphery of the lobule within the
interlobular septa.
Under normal conditions only a few of
these very thin septa will be seen.

13. There are two lymphatic systems: a
central network, that runs along the
bronchovascular bundle towards the
centre of the lobule and a peripheral
network, that is located within the
interlobular septa and along the pleural
linings.

14. The terminal bronchiole in the center divides into respiratory
bronchioli with acini that contain alveoli.
Lymphatics and veins run within the interlobular septa

15. Centrilobular area
It is the central part of the secondary
lobule.
It is usually the site of diseases, that
enter the lung through the airways
( i.e. hypersensitivity pneumonitis,
respiratory bronchiolitis, centrilobular
emphysema ).

16. Centrilobular area in blue
perilymphatic area in yellow

17. Perilymphatic area
Perilymphatic areais the peripheral part
of the secundary lobule.
It is usually the site of diseases, that are
located in the lymphatics of in the
interlobular septa ( i.e. sarcoid,
lymphangitic carcinomatosis, pulmonary
edema).
These diseases are usually also located
in the central network of lymphatics that
surround the bronchovascular bundle.

18. Raoof, S. , CHEST 2006; 129:805

20. 20

21. A group of terminal bronchioles
21

22. Accompanying pulmonary arterioles
22

23. Surrounded by lymph vessels
23

24. Pulmonary veins
24

25. Pulmonary lymphatics
25

26. 26
Connective Tissue StromaConnective Tissue Stroma

28. 28

30. In chest radiology, reticular and linear opacification refers to a
broad sub-group ofpulmonary opacification caused by a decrease in
the gas to soft tissue ratio caused by a pathological process centred in
and around the pulmonary interstitium. This includes thickening of
any of the interstitial compartments by blood, water, tumour, cells,
fibrous disease or any combination
fine "ground-glass" (1-2 mm): seen in processes that
thicken the pulmonary interstitium to produce a fine
network of lines, e.g. interstitial pulmonary oedema
medium "honeycombing" (3-10 mm): commonly seen
in pulmonary fibrosis with involvement of the
parenchymal and peripheal interstitium
coarse (> 10 mm): cystic spaces caused by parenchymal
descruction, e.g. usual interstitial pneumonia,
pulmonary sarcoidosis, pulmonary Langerhans cell histiocytosis

32. Focal irregular septal thickening in lymphangitic
carcinomatosis
Lymphangitic Carcinomatosis
results from hematogenous
spread to the lung, with
subsequent invasion of
interstitium and lymphatics.
The presenting symptoms are
dyspnea and cough and can
predate the radiographic
abnormalities.
In many cases however the
patients are asymptomatic.
Lymphangitic Carcinomatosis
is seen in carcinoma of the
lung, breast, stomach, pancreas,
prostate, cervix, thyroid and
metastatic adenocarcinoma
from an unknown primary.

37. usual interstitial pneumonia / idiopathic pulmonary fibrosis
(UIP/IPF)
non-specific interstitial pneumonia (NSIP)
cryptogenic organizing pneumonia (COP): formerly
bronchiolitis obliterans organizing pneumonia (BOOP)
respiratory bronchiolitis–associated interstitial lung disease
(RB-ILD)
desquamative interstitial pneumonia (DIP)
lymphoid interstitial pneumonia (LIP)
acute interstitial pneumonia (AIP): the only acute process in
the list

38. Typical UIP

39. Usual interstitial pneumonia
Usual interstitial pneumonia (UIP) is a form of lung disease characterized
by progressive scarring of both lungs.[1]
The scarring (fibrosis) involves the supporting
framework (interstitium) of the lung. UIP is thus classified as a form of
interstitial lung disease. The term "usual" refers to the fact that UIP is the most common
form of interstitial fibrosis. "Pneumonia" indicates "lung abnormality", which includes
fibrosis and inflammation. A term previously used for UIP in the British literature is
cryptogenic fibrosing alveolitis, a term that has fallen out of favor since the basic
underlying pathology is now thought to be fibrosis, not inflammation.
Location: distribution
The distribution of UIP on CT images is typically characteristically with an
apico-basal gradient with basal and peripheral predominance, although it is
often patchy.
Typical features include 1,5
:
the presence of reticular opacities in the immediate subpleural lung,
often associated with honeycombing and/ or traction bronchiectasis,

42. Traction bronchiectasis
Bronchial dilatation occurring as a consequence of interstitial
fibrosis is referred to as traction bronchiectasis (Figure 5). The
bronchi often appear irregular (corkscrewed) and are not associated
with radiologic evidence of bronchial inflammation (gross
bronchial wall thickening or mucous impaction). Traction
bronchiectasis is often accompanied by other signs of lung fibrosis
(honeycombing or irregular reticulation). While traction
bronchiectasis is quite specific for fibrosis, the differential
diagnosis is broader than that of honeycombing. Idiopathic
pulmonary fibrosis (IPF) is commonly associated with traction
bronchiectasis. However, in the absence of honeycombing, other
diseases are more likely (Chart 3). In patients with known collagen
vascular disease, bibasilar, peripheral, traction bronchiectasis
accompanied by ground-glass attenuation can be considered
diagnostic of NSIP. When the circumstances are less diagnostic, a
surgical biopsy might be required.

44. Honeycombing
Honeycomb lung remodeling (honeycombing) reflects the end stage
of a number of diseases that cause parenchymal destruction. It
presents a characteristic HRCT pattern, with subpleural, thick-
walled cysts that share walls and, when advanced, are often stacked
in multiple layers (Figure 6). It is typically accompanied by other
signs of fibrosis (traction bronchiectasis and reticulation).
Honeycombing is highly suggestive of a pathologic diagnosis of
usual interstitial pneumonia (UIP), although it can be attributable to
other diseases (Chart 3). Honeycombing seen on HRCT scans is
often considered diagnostic of UIP in patients presenting the
appropriate clinical profile, and the majority of such patients will
not be subjected to surgical lung biopsy. Because bilateral
honeycombing on HRCT scans is considered diagnostic under these
conditions, it is vitally important for the radiologist to be confident
that honeycombing is truly present before describing it.

45. NSIP

46. Non-specific interstitial pneumonia
-fibrotic non specific interstitial pneumonia: more common
-cellular non specific interstitial pneumonia: less common
Prognosis is much better when compared with UIP with 90% 5 years
survival rate for cellular and 45-90 % 5 years survival in fibrotic subtype.
Common manifestations include:
ground-glass opacities combined with irregular linear or reticular opacities
tends to be a dominant feature: can be symmetrically or diffusely distributed
in all zones or display a basal predominance
there can be relative subpleural sparing 11
- relatively specific sign
reticular opacities (sometimes - minor subpleural reticulation)
irregular linear opacities: with NSIP with fibrosis 6-7
thickening of bronchovascular bundles: with NSIP with fibrosis 6
scattered micronodules
in advanced disease
traction bronchiectasis
consolidation
microcystic honeycombing

48. Cardiogenic pulmonary edema (CPE) is defined as pulmonary
edema due to increased capillary hydrostatic pressure secondary
to elevated pulmonary venous pressure. CPE reflects the
accumulation of fluid with a low-protein content in the lung
interstitium and alveoli as a result of cardiac dysfunction .

51. CARDIOGENIC PULMONARY EDEMA

54. Drug toxicity disease can result in DILD, with histopathologic
reactions ranging from acute injury to UIP-like fibrotic
patterns.(36)
The mechanisms of drug-induced lung injury vary
from cytotoxicity to hypersensitivity
A wide variety of therapy-related reactions have been
described as a consequence of chemotherapeutic agents
(bleomycin, busulfan, chlorambucil, cyclophosphamide, 1,3-
bis(2-chloroethyl)-1-nitrosourea, and 1-(2-chloroethyl)-3-
cyclohexyl-1-nitrosourea), statins, amiodarone,
nitrofurantoin, methotrexate

55. All of the named rheumatic diseases can produce lung fibrosis. Rheumatoid
arthritis and scleroderma are predominately implicated in cases where a UIP
HRCT pattern is seen, and with similar functional abnormalities.

56. Radiation-induced lung disease (RILD) is a frequent complication of
radiotherapy to the chest for chest wall or intrathoracic malignancies and
can have a variety of appearances, especially depending on when the
patient is imaged. Acute and late phases are described, corresponding
to radiation pneumonitis and radiation fibrosisrespectively. These occur
at different times after completion of radiotherapy and have different
imaging features and differential diagnoses.

57. -Hypersensitivity pneumonitis
-Lymphoid pulmonary lesions
-Fibrosing sarcoidosis
-Asbestosis
DDX

58. THE END