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DR SHAROJ KHAN
MD Radiology RESIDENT
NMCTH
 Currently accepted classifications of pneumonia include:
 Community acquired pneumonia (CAP),
 hospital-acquired pneumonia (HAP),
 ventilator-associated pneumonia (VAP) and
 Health care–associated pneumonia (HCAP).
 A radiological pattern associated with homogenous fibrinosuppurative consolidation
of one or more lobes of a lung in response to a bacterial pneumonia
 A/K/A a non-segmental pneumonia or focal non-segmental pneumonia.
 M.C cause of lobar pneumonia is Streptococcus pneumonia
 -Other
 Klebsiella Pneumoniae
 Legionella Pneumophila
 Haemophilus Influenzae
 Mycobacterium Tuberculosis
 Consolidation in lobar
pneumonia mainly affect the
alveolar air spaces , there is
characteristic relative sparing
of the bronchi creating the
appearance of air bronchograms
 The lobar distribution of
consolidation occurs because of
spread of infection across
segmental boundaries , this is
facilitated by the pores of Kohn
and the canals of Lambert
On Radiograph -Homogenous
opacification in a lobar pattern -The
opacification can be sharply defined at the
fissures although more commonly there is
segmental consolidation -There may be
presence of air bronchograms and volume
loss in the affected areas.
CT : -Lobar pneumonia can have has a
pattern of focal ground-glass opacity in a
lobar or segmental pattern , this is due to
incomplete filling of alveoli and
consolidation -At times there can be dense
opacification of the entire lobe
Airspace opacity with air bronchograms obscuring the
right hemidiaphragm in keeping with right lower lobe
pnuemonia. Silhoutte sign
cervicothoracic sign
 a variation of the silhouette sign on frontal chest
radiography used to determine whether a superior
(para)mediastinal soft tissue mass is anterior or
posterior to the trachea.
 positive cervicothoracic sign - when thoracic lesion
contacts the neck or extends into it, thereby
obliterating the upper borders of the lesion on
radiographs.
 Because the anterior mediastinum ends at the level of
the clavicles, anterior mediastinal masses will
disappear as it ascends above the clavicle. Examples
include cystic hygroma, left superior vena cava, right
aortic arch, and thymic cyst .
 a lesion posterior to the trachea can have its upper
border outlined by lung above the level of the clavicles
(negative cervicothoracic sign), as the posterior
mediastinum ends much higher . Any lesion with a
discernible upper border above that level must be
located posteriorly in the chest,
 Thoracoabdominal sign
 Since the posterior costophrenic sulcus is more caudal than the anterior lung, a thoracic
lesion must be posterior if its caudal end is visible below the dome of diaphragm.
 convergence of the inferolateral border of the mass towards the spine suggests that the
mass is probably entirely intrathoracic (negative thoracoabdominal sign), whereas lack of
convergence or divergence indicates a segment silhouetted by the soft tissue density of
the abdomen (positive thoracoabdominal sign).
CT ‘angiogram sign’, initially described in the lobar form of lepidic adenocarcinomas as the enhancement
of branching pulmonary vessels in a homogeneous low-attenuation consolidation of lung parenchyma, may
also occur in lobar pneumonia.
Other diseases that manifest a
bulging fissure
include any space-occupying
process in the lung, such as
pulmonary hemorrhage, lung
abscess, and tumor.
 a type of pneumonia usually only seen in pediatric patients
 well defined rounded opacities that represent regions of infected consolidation
 mean age of patients with round pneumonia is 5 years and 90% of patients who
present with round pneumonia are younger than twelve
 infective agent in round pneumonia is bacterial (Streptococcus pneumoniae)
 most commonly occur in
superior segments of lower
lobes and in the majority of
cases (98%) , they are solitary.
 are round well circumscribed
parenchymal opacities , they
tend to have irregular margins
 Air bronchograms are often
present
 acute inflammation of the walls of the
bronchioles
 type of pneumonia characterized by multiple
foci of isolated acute consolidation affecting
one or more pulmonary lobules.
-Causative organisms include :
1-Staphylococcus Aureus
2-Klebsiella (often in debilitated patients and/or
alcoholics)
3-E.Coli
4-Pseudomonas (hospital acquired)
5-Haemophilus influenza (in children ,
immunocompromised adults) -Common hospital
acquired infection
Bronchopneumonia ,
confluent/merging parenchymal
consolidation with diffuse bilateral
pulmonary involvement (multiple
areas of consolidation)
c/b multiple small nodular or reticunodular opacities
which tend to be patchy and confluent
-This represents areas of lung where there are patches of
inflammation seperated by normal lung parenchyma -The
distribution is often bilateral and asymmetric and
predominantly involves the lung bases
 Multiple foci of opacity can be
seen in a lobular pattern centered
at centrilobular bronchioles.
 These foci of consolidation can
overlap to create a larger
hetrogenous confluent area of
consolidation -Exudates fill
airways = no air bronchograms
Image: Bilateral extended and exclusively peribronchial
dense infiltrations in the right upper lobe and lower lobe
as well as in the left lower lobe
Centrilobular nodules in a patient with bronchopneumonia A: Scattered ill-defined nodules
represent peribronchiolar consolidation and may contain a visible bronchiole (arrow) B: At
the lung bases , consolidated lobules surround air-filled bronchioles in several locations
 Refers to the radiological pattern associated with patchy inflammatory changes,
often confined to the pulmonary interstitium most commonly associated with
atypical bacterial etiologies :
 1-Mycoplasma Pneumoniae (most common) -In pediatric populations and in young
adults
 2-Chlamydophila Pneumoniae -In pediatric populations and in young adults
 3-Legionella Pneumophila (Legionnaires Disease)
Associated with immunocompromised patients and exposure to contaminated
aerosolised water (for example , from air conditioning system)
 Because the inflammation is
often limited to the
pulmonary interstitium and
the interlobular septa ,
atypical pneumonia has the
radiographic features of
patchy reticular opacities ,
these opacities are
especially seen in the
perihilar lung
1. A patient with Mycoplasma pneumonia , Chest radiograph
shows a vague ill-defined opacity in the left lower lobe
2. A Patient with Chlamydia pneumonia ,
Chest radiograph shows multifocal patchy
consolidation in the right upper , middle and
lower lobes
 Focal GGO in a lobular
distribution , involvement is
often diffuse and bilateral
 There may also be evidence
of pleural effusion
 Bronchial wall thickening
 Diffuse ground glass nodules
in a centrilobular pattern
are often present although
they progress to a soft tissue
density as the infection and
inflammation progresses
-In Mycoplasma pneumonia infection , airspace
consolidation is common , HRCT is sensitive for nodules
which are seen in 89% of patients
-In Legionella Pneumophila infection , residual scarring
may persist after resolution of the infection
 RADIOLOGICAL PATTERNS OF PULMONARY TUBERCULOSIS
 Radiological patterns may be considered under the following
groups:
 1. Typical radiological patterns of primary TB.
 2. Postprimary TB or phthisis.
 3. Patterns encountered in both primary and/or postprimary TB.
 4. Complications and sequelae of TB.
 5. Atypical patterns.
 Lymphadenopathy.
 Mediastinal and hilar lymphadenopathy is the
most common radiologic manifestation of
primary tuberculosis.
 Lymphadenopathy in tuberculosis typically
demonstrates a low-attenuation center with
peripheral rim enhancement on CECT images.
 Are due to central caseous necrosis with
peripheral granulomatous inflammatory
tissue.
 D/D of necrotic lymphadenopathy includes
nontuberculous mycobacterialinfection,
lymphoma, and metastatic carcinoma
 Parenchymal Disease
 Parenchymal disease most frequently manifests as consolidation depicted as an
area of opacity in a segmental or lobar distribution.
 no strong lobar predilection in primary tuberculosis.
 Cavitation occurs in a minority of patients with primary tuberculosis.
 when cavitation occurs, it is known as progressive primary disease.
 This cavitation occurs within existing consolidation and thus does not demonstrate
an upper lung zone predominance, in contrast to post primary disease.
 Parenchymal disease often appears similar to bacterial pneumonia, but the
presence of lymphadenopathy can be a clue that points toward primary
tuberculosis.
 Resolution of pulmonary consolidation is generally slow, taking as long as 2 years;
and in many cases, residual opacities are seen. After resolution, residual
parenchymal scarring can be seen at sites of prior consolidation in 15%–18% of
patients and is referred to as a Ghon focus, or Ghon tubercle
 Pleural Effusion
 seen in approximately 25% of primary tuberculosis cases in
adults, with the vast majority of such effusions being
unilateral.
 less common in postprimary disease.
 Tuberculous empyemas are typically loculated and
associated with pleural thickening and enhancement,
findings that represent involvement of the pleura.
 tuberculous empyemas may be complicated with
bronchopleural fistula or extension into the chest wall
(empyema necessitatis)
chest CT image shows
pleural calcifications
(arrowheads), a
loculated pleural effusion
with marked pleural
thickening, and
extension into the chest
wall (arrows).
 Airway Disease
 Bronchial wall involvement
may be seen in primary and
post primary tuberculosis,
although it is more common
in the former
contrast-enhanced reformatted chest CT image at the
level of the central bronchi shows irregular thickening of
the right upper lobe bronchus (arrow), as well as right
upper lobe volume loss
 Miliary Tuberculosis
 Hematogenous dissemination results in miliary
tuberculosis, especially in immunocompromised
and pediatric patients.
 Miliary disease may occur in primary or
postprimary tuberculosis.
 On the chest radiograph or CT image, miliary
disease manifests as diffuse 1–3-mm nodules in a
random distribution. Miliary tuberculosis is
spread by hematogenous seeding, as
demonstrated by the finding of a miliary nodule
centered on a small blood vessel
Axial chest CT image shows
numerous micronodules in a random
distribution. Note subpleural
(arrowhead) and centrilobular
(arrow) nodules
 Postprimary tuberculosis is typically thought to result from reactivation of dormant
M tuberculosis infection but may also result from a second infection with a different
strain, especially in endemic areas.
 The apical and upper lung zone predominance may be related to the relatively
reduced lymphatic drainage and increased oxygen tension in these regions, factors
that facilitate bacillary replication.
 A chest radiograph is typically obtained to evaluate for findings of active disease.
Chest CT may be useful in identifying active tuberculosis even if the chest
radiograph is negative, although chest CT is not the standard of practice
 Consolidation and Cavitation
 Patchy, poorly marginated consolidation is an early and consistent
feature of postprimary tuberculosis.
 apical and posterior segments of the upper lobes as well as the
superior segments of the lower lobe.
 Involvement of lung bases is rare (approx. 5%).
 In 3%–6% of cases, a non calcified nodule known as a tuberculoma
(ranging from 5 mm to 40 mm in largest dimension) may be the
predominant manifestation; these tuberculomas are typically
solitary and may occur with small satellite nodules
 In postprimary tuberculosis, cavitation is a common finding,
seen in 20%–45% of patients on chest radiographs.
 Cavities can be several centimeters in largest dimension and can
develop thick and irregular walls.
 Cavities with consolidation can be multi-focal.
 Residual cavities may persist after treatment, findings that
predispose to bacterial superinfection, mycetoma formation, or
erosion of adjacent vasculature resulting in hemoptysis. A
Rasmussen aneurysm is a rare life-threatening complication of
cavitary tuberculosis caused by granulomatous weakening of a
pulmonary arterial wall
 The presence of an air-fluid level within a cavity may be
related to the tuberculosis itself or to bacterial superinfection
 Centrilobular Nodules
 —Active tuberculosis often communicates
with the bronchial tree, which results in
endobronchial spread.
 Histologically, caseous necrosis and
granulomatous inflammation fill respiratory
bronchioles and alveolar ducts.
 This histologic finding manifests radiologically
as centrilobular nodules and the tree-in-bud
sign.
 Unlike cavitary lesions and consolidation,
centrilobular nodules may be seen in the
lower lobes, distant from the cavitary lesions
 Fungi involved in pulmonary infections are either pathogenic fungi, which can infect
any host, or saprophytic fungi, which infect only immunocompromised hosts.
 Pathogenic fungi cause
 coccidioidomycosis,
 blastomycosis and
 histoplasmosis.
 Saprophytes cause
 PCP,
 candidiasis,
 mucormycosis and
 aspergillosis.
 caused by Aspergillus sp., usually A. fumigatus.
 Classically, pulmonary aspergillosis has been categorised into saprophytic, allergic
and invasive forms.
 Aspergillus mycetomas are saprophytic growths that colonise a preexisting cavity in
the lung (usually sarcoidosis or tuberculosis).
 the disease type depends on an individual’s immune response
 As most cavities are due to
sarcoidosis or TB mycetomas these
tend to be located within the
upper lobes
 A fungal mass (mycetoma) within a
cavity with thickened walls
 may demonstrate a freely moving
fungus ball on decubitus imaging
 an ‘air crescent’ sign around the
mycetoma
 hypersensitivity reaction (type I) within the major airways leading to wall damage,
bronchiectasis and fibrosis
 elevated serum IgE
 common in asthma and cystic fibrosis
 CXR/CT: Consolidation (with or without a surrounding ground glass ‘halo’) ranging
from subsegmental to lobar involvement.
 consolidation clears, any residual bronchiectasis creates a favourable environment
for fungal recolonization
 atelectasis and occasionally cavitation are seen
Mucoid impaction: this obstructs the airways (the lung
parenchyma remains aerated by collateral drift,
permitting visualization of an impacted airway)
Finger in glove’ appearance: bronchoceles appearing as
branching thick tubular opacities pointing to the hilum
(finding is classically associated with allergic bronchopulmonary aspergillosis (ABPA),
seen in persons with asthma and patients with cystic fibrosis)
 •Bronchiectasis: this is permanent and indicates irreversible lung damage
 it affects the proximal bronchi more commonly than other bronchiectatic diseases
 there can be air trapping &‘Tree in bud’ appearance: mucoid impaction within dilated
bronchioles
 • Late disease: there is upper lobe fibrotic volume loss (the overall lung volume is
frequently increased due to lower lobe overinflation, small airway obstruction and
upper lobe bullae and cavitation)
 Chronic necrotizing (semi-invasive) aspergillosis: There is a normal or mildly
impaired immune status
 Invasive aspergillosis This affects immunocompromised hosts ▶ there is aggressive
vascular invasion and parenchymal necrosis (with a high mortality)
Mucoid impaction within bronchiectatic airways.
D/D Segmental bronchial atresia
This sign is seen in two types of Aspergillus infection:
angioinvasive and mycetoma
Air Crescent Sign
Aspergillus infection. Example of air crescent sign. Axial
(left) and coronal (right) CT images show air crescent
sign (arrows), which occurs in immunocompromised
patients with recovering neutrophil levels. Intracavitary
nodule (*) represents necrotic lung tissue
air crescent or Monad sign of mycetoma. Axial supine
(left) and prone (right) CT images show gravity
dependence of fungal ball (mycetoma). Air crescent sign
of mycetoma occurs in immunocompetent patients.
Fungus ball develops within preexisting cavity, usually in
association with tuberculosis or sarcoidosis.
Reverse Halo and Bird’s Nest Signs
peripheral consolidation surrounding a central area of
ground-glass opacity. Associated irregular and
intersecting areas of stranding or irregular lines may be
present within the area of ground-glass opacity and
become evident as the bird’s nest sign. These signs are
suggestive of invasive fungal infection (e.g.,
angioinvasive Aspergillus infection or mucormycosis) in
susceptible patient populations
D/D cryptogenic organizing pneumonia, bacterial
pneumonia, paracoccidioidomycosis, tuberculosis,
sarcoidosis, Wegener granulomatosis, and pulmonary
infarction
 CXR 3 patterns: •
 Pulmonary masses (which can be very large, are
usually single, have ill-defined edges, and which
may cavitate)
 Homogeneous segmental or lobar opacification
(+,- air bronchograms, cavitation and
lymphadenopathy)
 Diffuse nodular (occasionally miliary) or
reticulonodular opacities
CT Similar findings: ‘acinar’ nodules
 CXR/CT
 Multiple poorly defined nodules (5–
10mm)
 there is less commonly a segmental
or lobar pneumonia
3 patterns
• Chronic pulmonary histoplasmosis: this
resembles a postprimary tuberculosis:
• Histoplasmoma: a solitary well-
defined nodule
• the calcified centre forms a
‘target’ lesion (which is very
specific sign)
• Fibrosing mediastinitis: this may
occur with constriction of the
SVC and pulmonary vessels
 CXR •
 Consolidation, especially within the lower
lobes
 hilar/mediastinal adenopathy in 20% ▶ it
usually resolves •
 Chronic coccidioidomycosis occurs in 5% of
cases
 solitary/multiple nodules, which cavitate to
become thin-walled cavities
 Disseminated coccidioidomycosis is very
rare
 small nodules (5–10mm)
Chronic fibronodular cavitary disease may resemble post-
primary tuberculosis.
“Grape skin sign”
 CXR Areas of consolidation –
 multiple, patchy and bilateral •
 Cavitation and hilar adenopathy are very rare •
 Pleural effusion occurs in 25%
HYDATID DISEASE
Hydatid disease (echinococcosis) is a metazoal infestation caused by a tapeworm (usually
Echinococcus granulosus)
lung is the 2ND most common organ involved, after the liver, and is infected by either
hematogenous or direct transdiaphragmatic spread from the liver
• Cysts develop within the lungs (less commonly within the mediastinum) and are
usually solitary
• 10% of cysts are multiple, bilateral, or associated with liver cysts
• At presentation ⅔ of cysts are ruptured (⅓ remain intact)
‘Rising sun’/‘serpent’ sign: an essentially dry cyst with
crumpled membranes lying at its bottom
• The meniscus, Cumbo, and water lily signs are all seen
with pulmonary echinococcal infection
• These signs are caused by air dissecting between the
cyst layers, which are initially indistinguishable on CT
images because the cysts are fluid filled
• With bronchial erosion, air dissects between the outer
pericyst and ectocyst to produce the meniscus sign
It is believed that the meniscus sign is
suggestive of impending cyst rupture
• As it accumulates further, air penetrates
the endocyst layer and causes the Cumbo
sign, which comprises an air-fluid level in
the endocyst and a meniscus sign
• Finally, the endocyst layer collapses and floats on fluid,
forming the water lily sign/Camalote sign
• Rupture into the pleural space causes an effusion or, if
there is airway communication, a hydropneumothorax.
Empty cyst’ sign: a cyst with all its contents
expectorated
 zoonotic parasitic infection caused by lung flukes
 c/b Paragonimus westermani and Paragonimus
kellicotti
CXR Consolidation, nodules, band, tubular and ring
opacities (5–30mm) within any lobe (especially the
mid lung) ▶ pleural effusions are seen in up to 50%
of cases CT As above, but in addition peripheral
linear opacities (representing worm migration
tracks) may be seen
Burrow track sign
 usually occurs at the right lung base
with hemidiaphragmatic elevation,
and a pleural effusion (! thickening
and plate-like atelectasis)
pleuropulmonary amoebiasis is usually secondary to liver
involvement
 Influenza A.
 5%–10% of acute respiratory infections in
infants and children but for less than 1% of
respiratory illnesses in adults.
 Swyer–James–MacLeod syndrome is
considered to be a post-infectious
bronchiolitis obliterans (BO) secondary to
adenovirus infection in childhood.
CT findings in post-infectious BO consist of sharply
marginated focal areas of increased and decreased lung
opacity with reduced vessel size in lucent lung regions,
bronchial wall thickening and bronchiectasis. Air-
trapping is commonly visible on expiratory CT as lucent
areas that represent regions of lung that are poorly
ventilated and perfused.
Swyer James MacLeod syndrome with features of obliterative bronchiolitis
and it's sequel: hyperlucent right lower lobe, decreased vascular markings
and lobe volume, displaced fissures, bronchiolar wall thickening and
bronchiolectasis
 CT imaging features of SARS-CoV
infection consist of unilateral or
bilateral ground-glass opacities, focal
unilateral or bilateral areas of
consolidation or a mixture of both. In
the areas of ground-glass
opacification, thickening of the
intralobular interstitium or
interlobular septa may be present If
marked septal thickening occurs, a
‘crazy paving’ appearance results.
 All 3 of these disease caused by Corona virus. Since COVID/SARS and MERS are
considered from the same viral family (coronavirus), imaging features of COVID-19,
SARS, and MERS overlap, but still differences exist as well.
 Unlike SARS, where initial chest imaging abnormalities are more frequently
unilateral, COVID-19 is more likely to involve both lungs on initial imaging presented
as bilateral peripheral subpleural scattered ground-glass opacities.
 The majority of SARS positive patients show progressive multifocal distribution, in
the follow-up imaging, of which 75% of patients show bilateral distribution , while
MERS initial imaging tends to show multifocal airspace opacities in the lower lung
zones which then progress to extend peri-hilar and upper lobar.
 Pleural effusion is absent in COVID-19 patients while it is not rare in MERS and might
be observed in 20–33% of affected individuals.
 Pulmonary manifestation of HIV / AIDS
 Opportunistic infection
 Drugs reaction
 Immune restoration syndrome
 Lymphoproliferative disorders
 AIDS related malignancy
 Non-specific interstitial pneumonitis
 HIV related pulmonary hypertension
 Bronchiolitis obliterans
 Emphysema and bronchiectasis
 PNEUMOCYSTIS JIROVECI
 CXR 5–10% have a normal CXR at presentation
 positive findings include bilateral, diffuse, symmetrical, and fine to medium
reticular opacities
 usually there are no sequelae but pulmonary fibrosis can develop
 Pleural fluid or adenopathy is rare
 Pneumatocele: this affects 10% of patients they may rapidly increase or
decrease in size and then gradually resolve ▶ they appear within a few days and
can persist as a chronic thin-walled and air-filled cavity
 • Spontaneous pneumothorax (5%): this is due to multiple upper lobe
pneumatoceles
 • Unusual presentations: diffuse or focal miliary nodules ▶ homogeneous
opacities ▶ solitary or multiple wellformed nodules ▶ moderate to thick-walled
cavitary nodules • Upper lobe involvement is common as aerosolized
pentamidine may not reach the upper lobes (which can then resemble
reactivation TB)
 CT Unilateral or bilateral ground-glass or homogeneous opacities in a
geographical distribution
 Lung abscess
 Common causes of lung abscess include
anaerobic bacteria (most commonly
Fusobacterium nucleatum and
Bacteroides sp.), S. aureus, P.
aeruginosa and K. pneumoniae and
radiologically manifest with single or
multiple masses that are often
cavitated.
 Pulmonary gangrene
 is a rare complication of pneumonia characterised by the development of fragments of
necrotic lung within an abscess cavity (pulmonary sequestrum).
 Radiological manifestations consist initially of small lucencies within an area of
consolidated lung, usually developing within lobar consolidation associated with
enlargement of the lobe and outward bulging of the fissure (bulging fissure sign).
 Pneumatocele
 is a thin-walled, gas-filled space that usually
develops in association with infection.
 presumably results from drainage of a focus of
necrotic lung parenchyma followed by check-
valve obstruction of the airway subtending it,
enabling air to enter the parenchymal space
during inspiration but preventing its egress
during expiration.
 caused most often by S. aureus in infants and
children and P. jiroveci in patients who have
acquired immune deficiency syndrome (AIDS)
 Septic emboli
 to the lungs originate in
a variety of sites,
including cardiac valves
(endocarditis),
peripheral veins
(thrombophlebitis), and
venous catheters or
pacemaker wires. Feeding vessel sign is also recognized as a potential
manifestation of other conditions, including metastasis,
arteriovenous fistula, and pulmonary vasculitis
Arteriovenous fistula is differentiated from septic emboli by the finding not only of a feeding artery but
also of an enlarged draining vein.
 Empyema
 occurs in less than 5% of pulmonary infections.
 The pathogens traditionally associated with empyema are S. pneumoniae, Streptococcus
pyogenes and S. aureus.
 Radiographically, early signs include obliteration of the costophrenic angle. Complete
opacification of a hemithorax and contralateral mediastinal displacement may occur in
large effusions. Typically, an infected pleural effusion is encapsulated.
 Other CT features include (1) pleural enhancement and thickening of the parietal pleura
(split pleura sign), (2) increased density of extrathoracic fat and (3) thickening and
increased density of the extrapleural subcostal fat
 Bronchopleural fistula
 is a sinus tract between the bronchus and the pleural space that may result from
necrotising pneumonias, lung surgery, lung neoplasms and trauma.
 Imaging features consist of (1) increase in intrapleural air space,
 (2) appearance of a new air-fluid level,
 (3) changes in an already present air-fluid level,
 (4) development of tension pneumothorax and
 (5) demonstration of actual fistulous communication by CT.
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Imaging of pulmonary infections

  • 1. DR SHAROJ KHAN MD Radiology RESIDENT NMCTH
  • 2.  Currently accepted classifications of pneumonia include:  Community acquired pneumonia (CAP),  hospital-acquired pneumonia (HAP),  ventilator-associated pneumonia (VAP) and  Health care–associated pneumonia (HCAP).
  • 3.
  • 4.  A radiological pattern associated with homogenous fibrinosuppurative consolidation of one or more lobes of a lung in response to a bacterial pneumonia  A/K/A a non-segmental pneumonia or focal non-segmental pneumonia.  M.C cause of lobar pneumonia is Streptococcus pneumonia  -Other  Klebsiella Pneumoniae  Legionella Pneumophila  Haemophilus Influenzae  Mycobacterium Tuberculosis
  • 5.  Consolidation in lobar pneumonia mainly affect the alveolar air spaces , there is characteristic relative sparing of the bronchi creating the appearance of air bronchograms  The lobar distribution of consolidation occurs because of spread of infection across segmental boundaries , this is facilitated by the pores of Kohn and the canals of Lambert
  • 6. On Radiograph -Homogenous opacification in a lobar pattern -The opacification can be sharply defined at the fissures although more commonly there is segmental consolidation -There may be presence of air bronchograms and volume loss in the affected areas. CT : -Lobar pneumonia can have has a pattern of focal ground-glass opacity in a lobar or segmental pattern , this is due to incomplete filling of alveoli and consolidation -At times there can be dense opacification of the entire lobe
  • 7. Airspace opacity with air bronchograms obscuring the right hemidiaphragm in keeping with right lower lobe pnuemonia. Silhoutte sign
  • 8. cervicothoracic sign  a variation of the silhouette sign on frontal chest radiography used to determine whether a superior (para)mediastinal soft tissue mass is anterior or posterior to the trachea.  positive cervicothoracic sign - when thoracic lesion contacts the neck or extends into it, thereby obliterating the upper borders of the lesion on radiographs.  Because the anterior mediastinum ends at the level of the clavicles, anterior mediastinal masses will disappear as it ascends above the clavicle. Examples include cystic hygroma, left superior vena cava, right aortic arch, and thymic cyst .  a lesion posterior to the trachea can have its upper border outlined by lung above the level of the clavicles (negative cervicothoracic sign), as the posterior mediastinum ends much higher . Any lesion with a discernible upper border above that level must be located posteriorly in the chest,
  • 9.  Thoracoabdominal sign  Since the posterior costophrenic sulcus is more caudal than the anterior lung, a thoracic lesion must be posterior if its caudal end is visible below the dome of diaphragm.  convergence of the inferolateral border of the mass towards the spine suggests that the mass is probably entirely intrathoracic (negative thoracoabdominal sign), whereas lack of convergence or divergence indicates a segment silhouetted by the soft tissue density of the abdomen (positive thoracoabdominal sign).
  • 10. CT ‘angiogram sign’, initially described in the lobar form of lepidic adenocarcinomas as the enhancement of branching pulmonary vessels in a homogeneous low-attenuation consolidation of lung parenchyma, may also occur in lobar pneumonia.
  • 11. Other diseases that manifest a bulging fissure include any space-occupying process in the lung, such as pulmonary hemorrhage, lung abscess, and tumor.
  • 12.  a type of pneumonia usually only seen in pediatric patients  well defined rounded opacities that represent regions of infected consolidation  mean age of patients with round pneumonia is 5 years and 90% of patients who present with round pneumonia are younger than twelve  infective agent in round pneumonia is bacterial (Streptococcus pneumoniae)
  • 13.  most commonly occur in superior segments of lower lobes and in the majority of cases (98%) , they are solitary.  are round well circumscribed parenchymal opacities , they tend to have irregular margins  Air bronchograms are often present
  • 14.  acute inflammation of the walls of the bronchioles  type of pneumonia characterized by multiple foci of isolated acute consolidation affecting one or more pulmonary lobules. -Causative organisms include : 1-Staphylococcus Aureus 2-Klebsiella (often in debilitated patients and/or alcoholics) 3-E.Coli 4-Pseudomonas (hospital acquired) 5-Haemophilus influenza (in children , immunocompromised adults) -Common hospital acquired infection
  • 15. Bronchopneumonia , confluent/merging parenchymal consolidation with diffuse bilateral pulmonary involvement (multiple areas of consolidation) c/b multiple small nodular or reticunodular opacities which tend to be patchy and confluent -This represents areas of lung where there are patches of inflammation seperated by normal lung parenchyma -The distribution is often bilateral and asymmetric and predominantly involves the lung bases
  • 16.  Multiple foci of opacity can be seen in a lobular pattern centered at centrilobular bronchioles.  These foci of consolidation can overlap to create a larger hetrogenous confluent area of consolidation -Exudates fill airways = no air bronchograms Image: Bilateral extended and exclusively peribronchial dense infiltrations in the right upper lobe and lower lobe as well as in the left lower lobe Centrilobular nodules in a patient with bronchopneumonia A: Scattered ill-defined nodules represent peribronchiolar consolidation and may contain a visible bronchiole (arrow) B: At the lung bases , consolidated lobules surround air-filled bronchioles in several locations
  • 17.  Refers to the radiological pattern associated with patchy inflammatory changes, often confined to the pulmonary interstitium most commonly associated with atypical bacterial etiologies :  1-Mycoplasma Pneumoniae (most common) -In pediatric populations and in young adults  2-Chlamydophila Pneumoniae -In pediatric populations and in young adults  3-Legionella Pneumophila (Legionnaires Disease) Associated with immunocompromised patients and exposure to contaminated aerosolised water (for example , from air conditioning system)
  • 18.  Because the inflammation is often limited to the pulmonary interstitium and the interlobular septa , atypical pneumonia has the radiographic features of patchy reticular opacities , these opacities are especially seen in the perihilar lung 1. A patient with Mycoplasma pneumonia , Chest radiograph shows a vague ill-defined opacity in the left lower lobe 2. A Patient with Chlamydia pneumonia , Chest radiograph shows multifocal patchy consolidation in the right upper , middle and lower lobes
  • 19.  Focal GGO in a lobular distribution , involvement is often diffuse and bilateral  There may also be evidence of pleural effusion  Bronchial wall thickening  Diffuse ground glass nodules in a centrilobular pattern are often present although they progress to a soft tissue density as the infection and inflammation progresses -In Mycoplasma pneumonia infection , airspace consolidation is common , HRCT is sensitive for nodules which are seen in 89% of patients -In Legionella Pneumophila infection , residual scarring may persist after resolution of the infection
  • 20.
  • 21.  RADIOLOGICAL PATTERNS OF PULMONARY TUBERCULOSIS  Radiological patterns may be considered under the following groups:  1. Typical radiological patterns of primary TB.  2. Postprimary TB or phthisis.  3. Patterns encountered in both primary and/or postprimary TB.  4. Complications and sequelae of TB.  5. Atypical patterns.
  • 22.  Lymphadenopathy.  Mediastinal and hilar lymphadenopathy is the most common radiologic manifestation of primary tuberculosis.  Lymphadenopathy in tuberculosis typically demonstrates a low-attenuation center with peripheral rim enhancement on CECT images.  Are due to central caseous necrosis with peripheral granulomatous inflammatory tissue.  D/D of necrotic lymphadenopathy includes nontuberculous mycobacterialinfection, lymphoma, and metastatic carcinoma
  • 23.  Parenchymal Disease  Parenchymal disease most frequently manifests as consolidation depicted as an area of opacity in a segmental or lobar distribution.  no strong lobar predilection in primary tuberculosis.  Cavitation occurs in a minority of patients with primary tuberculosis.  when cavitation occurs, it is known as progressive primary disease.  This cavitation occurs within existing consolidation and thus does not demonstrate an upper lung zone predominance, in contrast to post primary disease.  Parenchymal disease often appears similar to bacterial pneumonia, but the presence of lymphadenopathy can be a clue that points toward primary tuberculosis.  Resolution of pulmonary consolidation is generally slow, taking as long as 2 years; and in many cases, residual opacities are seen. After resolution, residual parenchymal scarring can be seen at sites of prior consolidation in 15%–18% of patients and is referred to as a Ghon focus, or Ghon tubercle
  • 24.  Pleural Effusion  seen in approximately 25% of primary tuberculosis cases in adults, with the vast majority of such effusions being unilateral.  less common in postprimary disease.  Tuberculous empyemas are typically loculated and associated with pleural thickening and enhancement, findings that represent involvement of the pleura.  tuberculous empyemas may be complicated with bronchopleural fistula or extension into the chest wall (empyema necessitatis) chest CT image shows pleural calcifications (arrowheads), a loculated pleural effusion with marked pleural thickening, and extension into the chest wall (arrows).
  • 25.  Airway Disease  Bronchial wall involvement may be seen in primary and post primary tuberculosis, although it is more common in the former contrast-enhanced reformatted chest CT image at the level of the central bronchi shows irregular thickening of the right upper lobe bronchus (arrow), as well as right upper lobe volume loss
  • 26.  Miliary Tuberculosis  Hematogenous dissemination results in miliary tuberculosis, especially in immunocompromised and pediatric patients.  Miliary disease may occur in primary or postprimary tuberculosis.  On the chest radiograph or CT image, miliary disease manifests as diffuse 1–3-mm nodules in a random distribution. Miliary tuberculosis is spread by hematogenous seeding, as demonstrated by the finding of a miliary nodule centered on a small blood vessel Axial chest CT image shows numerous micronodules in a random distribution. Note subpleural (arrowhead) and centrilobular (arrow) nodules
  • 27.  Postprimary tuberculosis is typically thought to result from reactivation of dormant M tuberculosis infection but may also result from a second infection with a different strain, especially in endemic areas.  The apical and upper lung zone predominance may be related to the relatively reduced lymphatic drainage and increased oxygen tension in these regions, factors that facilitate bacillary replication.  A chest radiograph is typically obtained to evaluate for findings of active disease. Chest CT may be useful in identifying active tuberculosis even if the chest radiograph is negative, although chest CT is not the standard of practice
  • 28.  Consolidation and Cavitation  Patchy, poorly marginated consolidation is an early and consistent feature of postprimary tuberculosis.  apical and posterior segments of the upper lobes as well as the superior segments of the lower lobe.  Involvement of lung bases is rare (approx. 5%).  In 3%–6% of cases, a non calcified nodule known as a tuberculoma (ranging from 5 mm to 40 mm in largest dimension) may be the predominant manifestation; these tuberculomas are typically solitary and may occur with small satellite nodules
  • 29.  In postprimary tuberculosis, cavitation is a common finding, seen in 20%–45% of patients on chest radiographs.  Cavities can be several centimeters in largest dimension and can develop thick and irregular walls.  Cavities with consolidation can be multi-focal.  Residual cavities may persist after treatment, findings that predispose to bacterial superinfection, mycetoma formation, or erosion of adjacent vasculature resulting in hemoptysis. A Rasmussen aneurysm is a rare life-threatening complication of cavitary tuberculosis caused by granulomatous weakening of a pulmonary arterial wall  The presence of an air-fluid level within a cavity may be related to the tuberculosis itself or to bacterial superinfection
  • 30.
  • 31.  Centrilobular Nodules  —Active tuberculosis often communicates with the bronchial tree, which results in endobronchial spread.  Histologically, caseous necrosis and granulomatous inflammation fill respiratory bronchioles and alveolar ducts.  This histologic finding manifests radiologically as centrilobular nodules and the tree-in-bud sign.  Unlike cavitary lesions and consolidation, centrilobular nodules may be seen in the lower lobes, distant from the cavitary lesions
  • 32.
  • 33.  Fungi involved in pulmonary infections are either pathogenic fungi, which can infect any host, or saprophytic fungi, which infect only immunocompromised hosts.  Pathogenic fungi cause  coccidioidomycosis,  blastomycosis and  histoplasmosis.  Saprophytes cause  PCP,  candidiasis,  mucormycosis and  aspergillosis.
  • 34.  caused by Aspergillus sp., usually A. fumigatus.  Classically, pulmonary aspergillosis has been categorised into saprophytic, allergic and invasive forms.  Aspergillus mycetomas are saprophytic growths that colonise a preexisting cavity in the lung (usually sarcoidosis or tuberculosis).  the disease type depends on an individual’s immune response
  • 35.
  • 36.  As most cavities are due to sarcoidosis or TB mycetomas these tend to be located within the upper lobes  A fungal mass (mycetoma) within a cavity with thickened walls  may demonstrate a freely moving fungus ball on decubitus imaging  an ‘air crescent’ sign around the mycetoma
  • 37.  hypersensitivity reaction (type I) within the major airways leading to wall damage, bronchiectasis and fibrosis  elevated serum IgE  common in asthma and cystic fibrosis
  • 38.  CXR/CT: Consolidation (with or without a surrounding ground glass ‘halo’) ranging from subsegmental to lobar involvement.  consolidation clears, any residual bronchiectasis creates a favourable environment for fungal recolonization  atelectasis and occasionally cavitation are seen Mucoid impaction: this obstructs the airways (the lung parenchyma remains aerated by collateral drift, permitting visualization of an impacted airway) Finger in glove’ appearance: bronchoceles appearing as branching thick tubular opacities pointing to the hilum (finding is classically associated with allergic bronchopulmonary aspergillosis (ABPA), seen in persons with asthma and patients with cystic fibrosis)
  • 39.  •Bronchiectasis: this is permanent and indicates irreversible lung damage  it affects the proximal bronchi more commonly than other bronchiectatic diseases  there can be air trapping &‘Tree in bud’ appearance: mucoid impaction within dilated bronchioles  • Late disease: there is upper lobe fibrotic volume loss (the overall lung volume is frequently increased due to lower lobe overinflation, small airway obstruction and upper lobe bullae and cavitation)
  • 40.  Chronic necrotizing (semi-invasive) aspergillosis: There is a normal or mildly impaired immune status  Invasive aspergillosis This affects immunocompromised hosts ▶ there is aggressive vascular invasion and parenchymal necrosis (with a high mortality)
  • 41. Mucoid impaction within bronchiectatic airways. D/D Segmental bronchial atresia
  • 42. This sign is seen in two types of Aspergillus infection: angioinvasive and mycetoma Air Crescent Sign Aspergillus infection. Example of air crescent sign. Axial (left) and coronal (right) CT images show air crescent sign (arrows), which occurs in immunocompromised patients with recovering neutrophil levels. Intracavitary nodule (*) represents necrotic lung tissue air crescent or Monad sign of mycetoma. Axial supine (left) and prone (right) CT images show gravity dependence of fungal ball (mycetoma). Air crescent sign of mycetoma occurs in immunocompetent patients. Fungus ball develops within preexisting cavity, usually in association with tuberculosis or sarcoidosis.
  • 43. Reverse Halo and Bird’s Nest Signs peripheral consolidation surrounding a central area of ground-glass opacity. Associated irregular and intersecting areas of stranding or irregular lines may be present within the area of ground-glass opacity and become evident as the bird’s nest sign. These signs are suggestive of invasive fungal infection (e.g., angioinvasive Aspergillus infection or mucormycosis) in susceptible patient populations D/D cryptogenic organizing pneumonia, bacterial pneumonia, paracoccidioidomycosis, tuberculosis, sarcoidosis, Wegener granulomatosis, and pulmonary infarction
  • 44.  CXR 3 patterns: •  Pulmonary masses (which can be very large, are usually single, have ill-defined edges, and which may cavitate)  Homogeneous segmental or lobar opacification (+,- air bronchograms, cavitation and lymphadenopathy)  Diffuse nodular (occasionally miliary) or reticulonodular opacities CT Similar findings: ‘acinar’ nodules
  • 45.  CXR/CT  Multiple poorly defined nodules (5– 10mm)  there is less commonly a segmental or lobar pneumonia 3 patterns • Chronic pulmonary histoplasmosis: this resembles a postprimary tuberculosis: • Histoplasmoma: a solitary well- defined nodule • the calcified centre forms a ‘target’ lesion (which is very specific sign) • Fibrosing mediastinitis: this may occur with constriction of the SVC and pulmonary vessels
  • 46.  CXR •  Consolidation, especially within the lower lobes  hilar/mediastinal adenopathy in 20% ▶ it usually resolves •  Chronic coccidioidomycosis occurs in 5% of cases  solitary/multiple nodules, which cavitate to become thin-walled cavities  Disseminated coccidioidomycosis is very rare  small nodules (5–10mm) Chronic fibronodular cavitary disease may resemble post- primary tuberculosis. “Grape skin sign”
  • 47.  CXR Areas of consolidation –  multiple, patchy and bilateral •  Cavitation and hilar adenopathy are very rare •  Pleural effusion occurs in 25%
  • 48. HYDATID DISEASE Hydatid disease (echinococcosis) is a metazoal infestation caused by a tapeworm (usually Echinococcus granulosus) lung is the 2ND most common organ involved, after the liver, and is infected by either hematogenous or direct transdiaphragmatic spread from the liver • Cysts develop within the lungs (less commonly within the mediastinum) and are usually solitary • 10% of cysts are multiple, bilateral, or associated with liver cysts • At presentation ⅔ of cysts are ruptured (⅓ remain intact)
  • 49. ‘Rising sun’/‘serpent’ sign: an essentially dry cyst with crumpled membranes lying at its bottom • The meniscus, Cumbo, and water lily signs are all seen with pulmonary echinococcal infection
  • 50. • These signs are caused by air dissecting between the cyst layers, which are initially indistinguishable on CT images because the cysts are fluid filled • With bronchial erosion, air dissects between the outer pericyst and ectocyst to produce the meniscus sign It is believed that the meniscus sign is suggestive of impending cyst rupture • As it accumulates further, air penetrates the endocyst layer and causes the Cumbo sign, which comprises an air-fluid level in the endocyst and a meniscus sign • Finally, the endocyst layer collapses and floats on fluid, forming the water lily sign/Camalote sign • Rupture into the pleural space causes an effusion or, if there is airway communication, a hydropneumothorax. Empty cyst’ sign: a cyst with all its contents expectorated
  • 51.  zoonotic parasitic infection caused by lung flukes  c/b Paragonimus westermani and Paragonimus kellicotti CXR Consolidation, nodules, band, tubular and ring opacities (5–30mm) within any lobe (especially the mid lung) ▶ pleural effusions are seen in up to 50% of cases CT As above, but in addition peripheral linear opacities (representing worm migration tracks) may be seen Burrow track sign
  • 52.  usually occurs at the right lung base with hemidiaphragmatic elevation, and a pleural effusion (! thickening and plate-like atelectasis) pleuropulmonary amoebiasis is usually secondary to liver involvement
  • 54.  5%–10% of acute respiratory infections in infants and children but for less than 1% of respiratory illnesses in adults.  Swyer–James–MacLeod syndrome is considered to be a post-infectious bronchiolitis obliterans (BO) secondary to adenovirus infection in childhood. CT findings in post-infectious BO consist of sharply marginated focal areas of increased and decreased lung opacity with reduced vessel size in lucent lung regions, bronchial wall thickening and bronchiectasis. Air- trapping is commonly visible on expiratory CT as lucent areas that represent regions of lung that are poorly ventilated and perfused. Swyer James MacLeod syndrome with features of obliterative bronchiolitis and it's sequel: hyperlucent right lower lobe, decreased vascular markings and lobe volume, displaced fissures, bronchiolar wall thickening and bronchiolectasis
  • 55.
  • 56.
  • 57.
  • 58.  CT imaging features of SARS-CoV infection consist of unilateral or bilateral ground-glass opacities, focal unilateral or bilateral areas of consolidation or a mixture of both. In the areas of ground-glass opacification, thickening of the intralobular interstitium or interlobular septa may be present If marked septal thickening occurs, a ‘crazy paving’ appearance results.
  • 59.  All 3 of these disease caused by Corona virus. Since COVID/SARS and MERS are considered from the same viral family (coronavirus), imaging features of COVID-19, SARS, and MERS overlap, but still differences exist as well.  Unlike SARS, where initial chest imaging abnormalities are more frequently unilateral, COVID-19 is more likely to involve both lungs on initial imaging presented as bilateral peripheral subpleural scattered ground-glass opacities.  The majority of SARS positive patients show progressive multifocal distribution, in the follow-up imaging, of which 75% of patients show bilateral distribution , while MERS initial imaging tends to show multifocal airspace opacities in the lower lung zones which then progress to extend peri-hilar and upper lobar.  Pleural effusion is absent in COVID-19 patients while it is not rare in MERS and might be observed in 20–33% of affected individuals.
  • 60.  Pulmonary manifestation of HIV / AIDS  Opportunistic infection  Drugs reaction  Immune restoration syndrome  Lymphoproliferative disorders  AIDS related malignancy  Non-specific interstitial pneumonitis  HIV related pulmonary hypertension  Bronchiolitis obliterans  Emphysema and bronchiectasis
  • 61.  PNEUMOCYSTIS JIROVECI  CXR 5–10% have a normal CXR at presentation  positive findings include bilateral, diffuse, symmetrical, and fine to medium reticular opacities  usually there are no sequelae but pulmonary fibrosis can develop  Pleural fluid or adenopathy is rare  Pneumatocele: this affects 10% of patients they may rapidly increase or decrease in size and then gradually resolve ▶ they appear within a few days and can persist as a chronic thin-walled and air-filled cavity  • Spontaneous pneumothorax (5%): this is due to multiple upper lobe pneumatoceles  • Unusual presentations: diffuse or focal miliary nodules ▶ homogeneous opacities ▶ solitary or multiple wellformed nodules ▶ moderate to thick-walled cavitary nodules • Upper lobe involvement is common as aerosolized pentamidine may not reach the upper lobes (which can then resemble reactivation TB)  CT Unilateral or bilateral ground-glass or homogeneous opacities in a geographical distribution
  • 62.  Lung abscess  Common causes of lung abscess include anaerobic bacteria (most commonly Fusobacterium nucleatum and Bacteroides sp.), S. aureus, P. aeruginosa and K. pneumoniae and radiologically manifest with single or multiple masses that are often cavitated.
  • 63.  Pulmonary gangrene  is a rare complication of pneumonia characterised by the development of fragments of necrotic lung within an abscess cavity (pulmonary sequestrum).  Radiological manifestations consist initially of small lucencies within an area of consolidated lung, usually developing within lobar consolidation associated with enlargement of the lobe and outward bulging of the fissure (bulging fissure sign).
  • 64.  Pneumatocele  is a thin-walled, gas-filled space that usually develops in association with infection.  presumably results from drainage of a focus of necrotic lung parenchyma followed by check- valve obstruction of the airway subtending it, enabling air to enter the parenchymal space during inspiration but preventing its egress during expiration.  caused most often by S. aureus in infants and children and P. jiroveci in patients who have acquired immune deficiency syndrome (AIDS)
  • 65.  Septic emboli  to the lungs originate in a variety of sites, including cardiac valves (endocarditis), peripheral veins (thrombophlebitis), and venous catheters or pacemaker wires. Feeding vessel sign is also recognized as a potential manifestation of other conditions, including metastasis, arteriovenous fistula, and pulmonary vasculitis Arteriovenous fistula is differentiated from septic emboli by the finding not only of a feeding artery but also of an enlarged draining vein.
  • 66.  Empyema  occurs in less than 5% of pulmonary infections.  The pathogens traditionally associated with empyema are S. pneumoniae, Streptococcus pyogenes and S. aureus.  Radiographically, early signs include obliteration of the costophrenic angle. Complete opacification of a hemithorax and contralateral mediastinal displacement may occur in large effusions. Typically, an infected pleural effusion is encapsulated.  Other CT features include (1) pleural enhancement and thickening of the parietal pleura (split pleura sign), (2) increased density of extrathoracic fat and (3) thickening and increased density of the extrapleural subcostal fat
  • 67.  Bronchopleural fistula  is a sinus tract between the bronchus and the pleural space that may result from necrotising pneumonias, lung surgery, lung neoplasms and trauma.  Imaging features consist of (1) increase in intrapleural air space,  (2) appearance of a new air-fluid level,  (3) changes in an already present air-fluid level,  (4) development of tension pneumothorax and  (5) demonstration of actual fistulous communication by CT.

Editor's Notes

  1. Lymphadenopathy from primary tuberculosis in a 6-month-old male infant. Axial contrastenhanced chest CT image shows necrotic mediastinal lymphadenopathy (arrow) and a small rightsided pleural effusion.