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PAEDIATRIC CHEST
Dr Kamal Adhikari
Resident, MD Radiodiagnosis
NAMS
Imaging techniques
• Plain radiograph
• Barium swallow
• Fluoroscopy
• Computed Tomography
• MRI
• Ultrasonography
• Radionuclide imaging
• Bronchography/Angiography
Chest X-ray
• Basic investigation in childhood chest pathologies.
• Adequate inspiration – Right hemidiaphragm at the level of 8th rib
posteriorly.
• Expiration –
 Kink of trachea to right side.
 varying degree of opacification of lung fields.
Abnormal enlargement of heart.
• Differentiation between PA and AP film difficult.
• Difficulties in imaging – motion artefact and insufficient inspiration
• Need to consider some specific features in children:
Thymus
CTR – exceed usual 50%
Kink of trachea to right – If < full inspiration, tracheal kink to right.
Soft tissues – prominent in children e.g. anterior axillary fold crossing chest
wall can mimic pneumothorax.
 Plaits of hair over upper chest mimic infiltrations.
Pleural effusions – Seen as separation of lung from chest wall with relative
preservation of CP angle and accentuation of lung fissures.
Thymus
• Normal thymus in children – widened mediastinum.
• Lateral margin shows undulation – thymic wave.
• Towrads right, normal thymus may show triangular “sail-like”
configuration.
• Decreased size at stress and with steroids.
• Pathology identification can be difficult.
• USG helps – cystic lesions from homogenous normal thymus.
• MRI: Normal thymus homogenous SI while pathologies –
heterogenous.
• Fluoroscopy: Need to limit radiation exposure, pulsed rather than
continuous.
• Evaluation of differing radiolucencies in suspected foreign bodies.
• Obstructive emphysema: affected lung shows little volume change with
respiration, mediastinum shifts contralaterally on expiration.
• Lateral fluoroscopy: for dynamic evaluation of tracheomalacia.
• Barium swallow: Vascular rings, extrinsic masses, laryngeal clefts and
TOF.
• Either single contrast barium or water soluble contrast studies.
MRI
• Cardiac gated MR and MRA, assessment of cardiac lesions, great
vessels, mediastinal masses, tracheobronchial anomalies and
neurogenic masses.
Ultrasonography:
• Obviates the need for radiation.
• Evaluation of pleural fluid, pleural masses, peri diaphragmatic masses
and neck masses, pericardial disease, diaphragmatic pathologies,
evaluation of thymus.
• Antenatal ultrasonography – can identify the congenital pathologies
like sequestration.
• Bronchography:
• HRCT (thin sections) almost eliminated bronchography in children.
• Still used for functional bronchography and dynamics of
tracheobronchomalacia.
• Angiography:
• Therapeutic in bronchial artery embolization.
• In severe hemorrhage/ Hemoptysis in cystic fibrosis.
CT Scan
• Problems –
Cardiac and respiratory motion artefact.
 Less good tissue contrast due to paucity of mediastinal fat.
Ultrafast electron beam CT , Spiral CT and volumetric CT used – reduce
scan time  reduce need for sedation.
• HRCT –
Diffuse lung disease assessment.
Opportunistic lung disease assessment.
Road map for minimal invasive thoracic procedures.
Tracheobronchial abnormalities
Tracheal agenesis:
• Rare.
• Maternal polyhydramnios.
• Respiratory distress, absent cry and cannot intubate.
• 3 types:
Type I: No upper trachea, lower trachea Oesophagus
Type II: No trachea, common bronchus Oesophagus
Type III: Separate bronchi, separately connected to oesophagus.
Tracheal stenosis
• Acquired or congenital (rare).
• Following prolonged intubation or traumatic suctioning.
• Congenital stenosis d/t complete cartilaginous ring.
• Focal/generalized/funnel shaped.
• Funnel shaped d/t pulmonary artery sling.
• Presentation: 1st year of life with biphasic stridor.
• Bronchoscopy, CT, MRI.
• Associated anomalies: Tracheo-esophageal fistula, pulmonary
agenesis or hypoplasia, pulmonary artery sling and bronchial stenosis.
Tracheal stenosis. A, Axial CT shows severe narrowing of the
trachea at the level of thoracic inlet (arrow) approximately 7
cm from the glottis. B, Coronal MiniP image shows severe
narrowing (arrow) at the level of thoracic inlet.
Tracheomalacia
• Expiratory collapse of trachea due to softening of tracheal wall.
• Secondary to: Cartilagenous anomalies.
Tracheostomy.
Oesophageal atresia or TOF.
Chronic inflammation (cystic fibrosis, recurrent aspiration,
immunodeficiency).
Extrinsic compression (vascular rings, slings or aberrancy).
Neoplasia.
• Expiratory wheeze,
exacerbated with crying,
normal at rest.
• Lateral fluoroscopy:
Exaggerated decrease in
sagittal width of trachea
during expiration.
• Dynamic CT: assess cross
sectional anatomy and
compliance of trachea.
Tracheomalacia. Radiograph of the trachea in a 2-month-old
infant with stridor shows marked diffuse tracheal narrowing
during expiration (arrows). Radiographs of a 3-week-old infant
with Hurler disease
Tracheo-oesophageal fistula
• Choking, cyanosis, coughing at feeding, insidiously as chronic
respiratory infection.
• Oesophageal atresia – obvious diagnosis.
• Majority associated with oesophageal atresia.
• If not, diagnosis difficult.
• Contrast oesophagogram: Fine hair-like structure connecting
oesophagus and trachea with linear opacification of posterior
tracheal wall.
• Type A - Esophageal atresia without fistula so-called pure esophageal atresia (10%)
• Type B - Esophageal atresia with proximal TEF
• Type C - Esophageal atresia with distal TEF (85%)
• Type D - Esophageal atresia with proximal and distal TEFs
• Type E - TEF without esophageal atresia or so-called H-type fistula (4%)
Bronchial atresia
• Upper lobe bronchi frequently atretic.
• Newborn: Mass occupying part or all of an upper lobe (fetal lung fluid
trapped behind the atresia).
• Later, fetal lung fluid escapes via pores of kohn/canals of lambert –
round opacity central to air trapping.
• Associations: Bronchogenic cyst, intralobar sequestration or cystic
adenomatoid malformation.
Bronchial atresia. Axial CT shows an area of mucoid plugging in
the left lower lobe (white arrow), and distal to this there is an
area of hyperlucency (black arrow), consistent with bronchial
atresia.
Tracheal bronchus
• also known as PIG bronchus.
• 1% of normal population.
• right upper lobe bronchus directly arises from the trachea.
Tracheal bronchus. Coronal CT shows the tracheal bronchus
(bronchus suis) (arrow) originating from the trachea and
supplying the right upper lobe.
Congenital pulmonary venolobar syndrome
• Scimitar syndrome
• Congenital aplasia or hypoplasia of one or more lobes of right lung.
• Other variable features:
Partial anomalous pulmonary venous return
Anomalous or rudimentary arterial supply of the hypolplastic lobes
(small pulmonary artery or supply directly from thoracic
aorta/abdominal aorta/celiac axis).
Hemidiaphragm abnormality
Small hemithorax, obscuration of heart border, retrosternal soft
tissue density.
• AP view: Anomalous vein has “Turkish Scimitar” shape, drains into IVC
or even hepatic vein or portal vein or right atrium.
• May be association with pulmonary sequestration (right lower lobe) –
appears as mass of abnormal lung tissue.
Lung Agenesis
• Small opaque hemithorax, ipsilateral
mediastinal shift
• Presentation: Neonatal respiratory
distress. Can even present in
adulthood, radiologically as “White-
out” hemithorax.
• Bronchography/Bronchoscopy:
Absent mainstem bronchus
• Angiography: No pulmonary or
bronchial artery circulation.
• Association: VATER syndrome
• D/D: Pulmonary hypoplasia and
complete lung atelectasis
Pulmonary Hypoplasia
• Factors compromising thoracic space available for lung growth.
• Intrathoracic: diaphragmatic hernia or extralobar sequestration
• Extrathoracic: Oligohydramnios/arthrogryphosis
• Classically right lung involved.
• Right sided obstructive heart disease
• Association: Diaphragmatic hernia, renal agenesis/dysgenesis
• Imaging:
• Decrease in volume of right hemithorax.
• I/L mediastinal shift.
• Obscuration of heart border d/t extrapleural areolar tissue.
Congenital Lobar Overinflation/emphysema
• Progressive overdistension of a lobe or may be 2 lobes.
• Emphysema – misnomer, no alveolar wall destruction.
• Cause: Ball-valve mechanism obstruction of bronchus
Abnormal bronchial cartilage deficiency/dysplasia
Inflammatory changes Wall abnormality
Inspissated mucus
Mucosal folds/webs Intraluminal
Broncial stenosis
Extrinsic vascular or mass compression Extraluminal cause
• M:F = 3:1
• Associated anomalies: Cardiovasular up to 50%, PDA, VSD and TOF
• Lobar involvement: Upper lobes or right middle lobe
• Left upper – 43%, Right middle – 32%, right upper – 20%, lower lobes
– 5%.
• Radiography:
• Neonate: Fluid may get trapped, opaque enlarged hemithorax.
• Later, fluid resorption, grossly overinflated lobe with generalized
hypertransradiancy, marked attenuation of pulmonary vessels,
compression of adjacent lobes.
Congenital lobar emphysema/overinflation. Chest X-ray
shows gross overinflation of the right lung which is hypovascular
with marked shift of the mediastinum to the left and herniation of
the lung into the left hemithorax (arrow). (B) CT of right middle
lobe congenital lobar overinflation/emphysema causing shift of
the mediastinum to the left with marked distortion of the pleural
reflections to the left of the midline.
Hyperexpansion of the left upper lobe
with a portion herniated across the
midline. There is shift of the
mediastinum to the right, flattening of
the left hemidiaphragm and some
compression of the left lower lobe.
Bronchopulmonary foregut malformations
• Developmental anomalies from abnormal budding of the embryonic
foregut and trachea-bronchial tree.
Foregut cysts
Bronchogenic cysts
Enteric and neurenteric cysts
Cystic hamartomatous adenomatoid malformation
Pulmonary sequestration
Bronchogenic cysts
• ½ of all congenital thoracic cysts
• Intrapulmonary or mediastinal (>common, earlier budding
abnormality)
• Lined by ciliated epithelium, may contain smooth muscle and
cartilage
• Mediastinal cysts: paratracheal (right sided >), carinal (m/c) or hilar
• No communication with tracheobronchial tree
• Instrumentation or infection – air-fluid level or air filled cyst.
• D/D – Acquired cyst, cystic mesenchymal hamartoma.
CT: Large fluid density lesion in
right superior mediastinum, no
invasion into mediastinum or
lung
Coronal T2-weighted image in the same
patient shows a hyperintense lesion (arrow)
splaying the carina.
Enteric cysts
• Early embryogenesis
• Located in posterior mediastinum
• If in oesophageal wall, oesophageal
cysts or duplication cysts.
• Can present early with acid
secretion, may rupture into
tracheobronchial tree leads to
hemoptysis.
• Large posterior mediastinal mass
(right-sided).
• Tc-MDP scan, uptake – gastric
mucosa.
Esophageal duplication cyst in a 3-year-old girl with
cough and dyspnea. (a) Chest radiograph shows
homogenous opacification of the right hemithorax
(arrows) at the time of first admission. (b) Follow-up
CT scan 3 years later shows a large cystic
periesophageal mass (arrows)
Neuroenteric cysts
• Posterior mediastinal masses with associated vertebral abnormalities.
• MRI needed to evaluate thoracic or spinal components of these cysts.
• Foregut cysts can have water attenuation or even increased
depending on viscousity of content.
• CT attenuation or MRI intensity varies.
• Usually unilocular and no enhancement.
Neurenteric cyst in female patient with flank pain. (a) Chest radiograph shows a well-defined round mass (arrow)
in the lower thoracic region. (b- c) Both axial T1-weighted – and coronal T2-weighted MR images show a large
mass that is of homogenous high signal intensity in the right paravertebral region (arrow). The cyst presumably
contains proteinaceous fluid. (d) The photograph of the resected tumor shows a thick-walled encapsulated cystic
mass.
Congenital Cystic Adenomatoid Malformation
• Hamartomatous proliferation of terminal bronchioles at the expense of
alveolar development.
• Lesions composed of both cystic and solid components.
• Cysts communicate with tracheobronchial tree.
• Predilection for upper lobes.
• Type I: m/c, 50%, variable cysts, at least 1 cyst > 2 cm d, < 5% congenital
anomalies.
• Type II: 41%, smaller, uniform cysts < 2 cm, 50% children anomalies (renal,
intestinal, skeletal, cardiac)
• Type III: microcysts, solid in gross, fetal hydrops and polyhydramnios,
associated congenital anomalies, poor prognosis.
Modified Stocker CPAM
Type Description
• 0 Incompatible with life
• 1 Commonest type (>65%)
Several large intercommunicating cysts (up to 10 cm)
Mediastinal shift is common
• 2 10–15% of cases
Smaller than other types
Small evenly sized cysts (up to 2 cm)
Often associated with other congenital abnormalities
• 3 ~8% of cases
Large solid lesion with small cysts (1.5 cm)
Nearly always causes mediastinal shift
Poor prognosis
• 4 10–15% of cases
• Large cysts (up to 7 cm) ,May be associated with, or a precursor of pleuropulmonary blastoma
Cystic adenomatoid malformation. A, Axial CT shows large
cystic spaces filled partially with fluid in the medial aspect of
the right upper lobe. B, Axial CT shows multiple small cystic
lesions in the left lower lobe in type 2 CPAM. C, Coronal CT in
same patient shows multiple small cystic lesions in the left
lower lobe.
Type I cyst: Multiple air filled cysts
in left hemithorax, thin walled
cysts, C/L mediastinal shift.
CT: similar findings
Chest X-ray: right cystic hamartomatous/adenomatous
malformation type 1 with multiple cystic lesions in the right lower
lobe showing air-fluid levels consistent with infection. (B) Axial CT
scan through the lung bases show the thick-walled cysts in the right
lower lobe.
Pulmonary Sequestration
• Congenital mass of aberrant pulmonary
tissue that has no normal connection
with the bronchial tree or with the
pulmonary arteries.
• Artery: usually anomalous, from aorta
• Vein: Azygous system, pulmonary veins
or IVC
• Types: Intralobar and extralobar
• Usually asymptomatic, m/c
presentation is recurrent pneumonia.
Imaging in sequestration
• Identify sequestrated or dysplastic lung
• Identify aberrant arterial or venous connections
• Identify possible bronchial or gastrointestinal connections
• Exclude other associated lung anomalies, horse-shoe lung or
hypoplasia
• Assess diaphragm integrity
• Identify other associated anomalies
Contd..
• Ultrasonography: Neonate – mass adjacent to liver or diaphragm
• Antenatal USG: fetal chest mass with Doppler showing vascular
connections to the sequestration.
• CT:
• Intralobar - Multicystic mass at lung bases
• Extralobar – Soft tissue mass with avid contrast enhancement
adjacent to diaphragm
• MRI: Identification of pulmonary abnormality and vascular
connections in multiplanar.
Intralobar sequestration
• >common, 70-85%
• Within lung, no separate pleural covering, intimately connected to
adjacent lung.
• Venous drainage via pulmonary veins.
• Location: lower lobes (98%), medial part of left lower lobe – m/c.
• Anomalies <12%.
• Diagnosis at adolescence with recurrent or refractory pneumonia.
2 round opacities overlying the left
cardiac border. They have no silhouette
with the left cardiac border, left
diaphragm or descending aorta
suggesting the left lower lobe location.
Mass in the left lower lobe with soft tissue
density (26 HU) , with defined border and
peripheral calcification. No visceral pleura
around the mass. No enhancement. arteries
directly from aorta, vein drain into
pulmonary v
well defined wedge shaped
echogenic lesion in right lower
lung. D/D – CPAM III , separate
feeding vessel from aorta
Extralobar Sequestration
• Less common, 15-25%
• Extrapleural, can be intrathoracic or extrathoracic, almost always left lower
lobe
• Presentation- early, neonate with cyanosis, respiratory distress, infection
• M:F = 4:1.
• Venous drainage via systemic veins into right atrium
• Separated from surrounding lung by own pleural covering.
• Associations: 65% - Pulmonary hypoplasia, horse-shoe lung, CCAM,
bronchogenic cysts, diaphragmatic hernia and CVS anomalies (TA and
TAPVR).
Left sided extralobar sequestration with a large
systemic vessel from aorta, coronal CT shows,
normal lung, beneath which left sided basal ELS
and draing vein into azygous below diaphragm
CHARACTERSTIC INTRALOBAR EXTRALOBAR
Incidence More common ( 75 %) Less common( 25 %)
Gender predisposition Equal Men 4: 1
Pleural investment Shares visceral pleura of parent
lobe
Separate visceral pleura
Location Lower lobes(98%) , medial part
of the left lobe
Above, below or within
diaphragm
Venous Drainage Pulmonary venous Systemic venous (azygos, IVC,
portal)
Presentation Early adulthood with a history
of pulmonary infection, chronic
cough, or asthma.
Asymptomatic mass (15%)
Mostly present during first 6
months of life
due to respiratory or
feeding problems
Radiographic
Features
Homogeneous
consolidation with
irregular margins or
uniformly dense mass
with smooth or lobulated
contours.
Single well defined,
homogeneous, triangular
shaped opacity in the lower
thorax. May present
else where in the thoracic
cavity.
DIAPHRAGMATIC ABNORMALITIES
• Hernia
• Eventeration
• Agenesis
• These anomalies associated with lung malformations and cause
severe respiratory symptoms
Bochdalek’s hernia
• Through the posteropleuoperitoneal foramen.
• Causes severe respiratory distress in the neonate .
• Involves the left pleuroperitoneal foramen in 75 % of cases.
• Neonatal radiograph shows a left-sided large intrathoracic mass of
soft-tissue density
• There is absence of the normal gas-containing bowel in the abdomen
which is usually scaphoid on examination and other developmental
abnormalities of the lung.
• Prognosis depends on degree of underlying lung hypoplasia.
The differential diagnoses are of other cystic-appearing intrathoracic
masses in the newborn
• Lobar emphysema,
• Cystic adenomatoid malformations.
• Sequestration,
• Bronchogenic cysts
2 days old child showing a left-sided
congenital diaphragmatic hernia
with loops of bowel in the left
hemithorax and shift of the heart
and mediastinum to the right
Lateral chest X-ray shows bulge in diaphragmatic contour just
above posterior costophrenic recess. CT shows fatty mass
abutting the defect in posteromedial aspect of left
hemidiaphragm.
Congenital eventeration of the diaphragm
• Either partial or complete
• Nearly always left sided, due to
hypoplasia of the diaphragmatic
muscle.
• Most eventerations are minor,
transitory, local diaphragmatic
elevations found incidentally
within the first few years of life
Frontal and lateral chest x-ray shows smooth elevation of right
hemidiaphragm medially and anteriorly consistent with an
eventeration of the hemidiaphragm
Newborn chest
Immature lung disease
• Small, premature infants with clinical, radiological and prognostic features
differing from respiratory distress syndrome (RDS).
• Birth weight < 1500 gms.
• UNLIKE RDS, respiratory distress not seen until first 4-7 days.
• Insufficient surfactant.
• CXR: diffuse granularity of lungs, with relative absence of air bronchograms
and little or no underaeration of lungs (unlike in RDS).
• Complications: apnoea and bradycardia, persistent PDA
• Need ventillatory support
• Better prognosis compared to RDS (overall survival of 82%)
Respiratory Distress Syndrome
• Immaturity
• <2.5 kgs, <36 weeks gestation
• Leading cause of death in newborns
• Symptoms shortly after birth, chest wall retraction, cyanosis, grunting
• Deficiency of pulmonary surfactant.
• hallmark features: reticular granularity of the lungs due to superimposition
of multiple acinar nodules, related to atelectatic alveoli and diffuse
pulmonary under aeration.
• Air bronchograms due to coalescence of areas of atelectasis around dilated
terminal bronchioles
• Pulmonary interstitial emphysema: due to rupture of alveolar air sacs
Hyaline membrane disease. (A) Mild changes aged 1 day-fine
reticulonodular shadowing with prominent air bronchograms.
(B) More advanced changes aged 3 days-marked pulmonary
opacification with loss of diaphragmatic and cardiac contours.
Pulmonary Interstitial Emphysema
• also known as air block phenomenon.
• almost always preceded by postitive pressure ventilation.
• increase in transalveolar pressure leading to alveolar rupture
,dissection of air along peribronchial and perivascular spaces of
interstitium.
• tortuous linear luciencies of uniform size radiating from the hila
through the lungs.
• occurs in first week(CLD of prematurity usually in second week).
Pulmonary interstitial emphysema. Fine reticular
Shadowing in the right lung with deviation of the mediastinum
contralaterally. RDSaffecting the left lung.
Bilateral pneumothoraces in
hyaline membrane disease. Right
intercostal drain.
Bronchopulmonary dysplasia or chronic lung
disease of prematurity
• Complication of ventilation in newborn.
• Prolonged oxygen or ventilator therapy to developing lung.
• 4 stages of progression:
Stage I - ~ ARDS
Stage II: 4-10 days, Bilateral “white-outs” (necrosis, epithelial repair
with hyaline membrane, interstitial edema)
Stage III: 10-20 days, Bubbly appearance of lung (alveolar
overdistension)
Stage IV: after 1 month, Classic bubbly appearance with alternating
cyst like lucencies surrounded by curvilinear stranding of soft tissue.
Bronchopulmonary dysplasia. Patchy
shadowing from areas
of loss of volume and fibrosis, with areas of
compensatory emphysema,
especially in the right upper lobe.
Bilateral ill-defined reticulonodular markings, more prominent on the right,
with obscuration of the right hemidiaphragm and heart border, positive air-
bronchograms and hyperinflation of the left lower zone. No apparent atelectasis
Bronchopulmonary dysplasia (BPD). A, Axial CT in a patient with BPD shows heterogeneous attenuation containing
high attenuation and also areas of low attenuation. B, Axial CT shows bilateral multiple small cystic lesions in lungs of a
patient with BPD.
Transient tachypnea of newborn or wet lung
disease
• Delayed clearance and resorption of lung
fluid.
• Series of changes in X-ray:
• First 6 hrs, fluid within lungs with increased
vascular markings and hazy margins.
• AT 10-12 hrs, gradual clearance, reticular
granular densities ( ~ in RDS) but no
underinflation of lungs.
• At 48-72 hrs, gradual clearance from center to
periphery.
Meconium Aspiration Syndrome
• Cause: intrauterine or intrapartum aspiration of
meconium
• Secondary to intra-uterine hypoxemia
• Leads to bronchial obstruction and chemical
pneumonitis.
• Bilateral patchy asymmetrical areas of
opacification with marked overinflation.
• Complication: Pneumothorax and
pneumomediastinum.
• Radiological improvement lags behind clinical
improvement.
Meconium aspiration. There is marked overinflation
of the lungs with coarse nodular shadowing
secondary to meconium aspiration.
Bilateral chest drains drain pneumothoraces
Chest radiograph in a older child
Pulmonary infections
• Viral infections > bacterial
• Air trapping or atelectasis > common in children < 8 yrs (small caliber
peripheral airways, more collapsible and more mucus gland lining the
airways)
• Role of imaging: Confirm the presence, localization, extent and
complication.
• Not specific for specific organism.
Tuberculosis
• Primary TB causes localized air space disease (segmental or lobar) and
regional node enlargement.
• Occasionally, pleural effusion.
• Caseation and necrosis of lymph node or inflammatory focus can
occur (weeks later).
• Resistance leads to involution or calcification .
• Poor resistance or overwhelming infection, extension, larger area of
lung involvement with effusion.
• From lymphatic to venous system via thoracic duct leads to milliary
nodules.
6 yr boy, presentation X-ray shows, tuberculoma right
lower lung, f/u X-ray 4 yr later, parenchymal calcification
with calcified nodes
Interstitial granular densities distributed
throughout the lungs, with relative basal and
apical sparing. No pleural effusions. No loss of
volume.
Inhaled foreign body
• May be radiopaque or non-radiopaque
• Tend to enter right main bronchus
• Complete obstruction – peripheral collapse
• Incomplete obstruction – obstructive emphysema
• Films in expiration or decubitus position and inspiration, if needed
fluoroscopy, mediastinal shift away from obstructive emphysema on
expiration/decubitus position (abnormal lung dependent).
• If clinical suspicion (negative radiograph) – Bronchoscopy.
Foreign body inhalation. (A) Obstructive emphysema from a
foreign body in the left main bronchus. (B, C) Another child
showing loss of volume in the left lung with patchy collapse in
the apex of the left lower lobe; in inspiration (B) the
mediastinum is slightly to the left; in expiration (C) the volume
of the left lung changes little with the mediastinum swingi
ng to the right.
Cystic fibrosis
• 2nd m/c chronic respiratory illness among children and young adults.
• Chr 7, cystic fibrosis gene, Autosomal recessive.
• Infants – atelectasis, focal or generalized overinflation with mucus
plugging partially obstructing the airway.
• Initial feature similar to viral pneumonitis.
• Older children – overinflation, bronchial wall thickening, dilatation
and mucus plugging – bronchiectasis.
• Bronchiectatic cavities – air-fluid levels.
• Hilar adenopathy, pulmonary hypertension.
• HRCT – Early changes, hallmark – extensive central bronchiectasis.
• Complication assessment:
• Pneumothorax
• Hemoptysis – source of bleeding identified by bronchial
arteriography.
• Cor-pulmonale and pulmonary hypertension.
Bilateral predominantly upper lobes bronchiectasis​ with
patchy consolidations and mild hyperinflation.
Bilateral severe, widespread bronchiectasis with occasional
mucus plugging and background mosaic attenuation, most likely
due to air trapping. Lung volumes are increased.
Cystic fibrosis. A, Coronal CT in a patient with cystic fibrosis shows extensive cystic bronchiectatic changes
predominantly seen in the upper lobes, along with bronchial thickening. The lungs are hyperinflated. B, Axial CT
in the same patient shows extensive bilateral upper lobe–predominant bronchiectatic changes along with
bronchial thickening and areas of mucoid plugging.
Idiopathic pulmonary haemosiderosis
• Unknown aetiology.
• Intra-alveolar hemorrhage.
• Acute hemorrhage – bilateral hazy
opacification ~ pulmonary edema
• After blood clears up, hemosiderin
deposited in lung septa – reticulonodular
interstitial pattern.
• Diagnosis: hemosiderin laden macrophages
in sputum.
Idiopathic pulmonary haemosiderosis. Perihilar
shadowing with a reticulonodular pattern in the
peripheral lung fields.
Pulmonary alveolar proteinosis
• Lipoprotenaceous deposits in alveolar spaces
• M;F – 2:1, ~ 20 years of age.
• CXR: multiple acinar nodules in miliary pattern, may coalesce, larger
areas of consolidation.
• CT: nodules more in dependent lung portions
• Histology: PAS positive staining
Fig. 9.25 (A) Pulmonary alveolar proteinosis. Chest X-ray showing
diffuse alveolar shadowing in a perihilar distribution with some fine
linear change in the upper zones. (B) High-resolution CT scan
confirming these appearances showing diffuse alveolar exudate with
interstitial thickening most marked in the non-dependent areas of
the lung.
References
• Textbook of Radiology and Imaging, David Sutton.
• RSNA articles Primary tuberculosis in childhood: radiographic
manifestations.
• Images from different web search.
Paediatric chest  by Dr. Kamal

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Paediatric chest by Dr. Kamal

  • 1. PAEDIATRIC CHEST Dr Kamal Adhikari Resident, MD Radiodiagnosis NAMS
  • 2. Imaging techniques • Plain radiograph • Barium swallow • Fluoroscopy • Computed Tomography • MRI • Ultrasonography • Radionuclide imaging • Bronchography/Angiography
  • 3. Chest X-ray • Basic investigation in childhood chest pathologies. • Adequate inspiration – Right hemidiaphragm at the level of 8th rib posteriorly. • Expiration –  Kink of trachea to right side.  varying degree of opacification of lung fields. Abnormal enlargement of heart. • Differentiation between PA and AP film difficult. • Difficulties in imaging – motion artefact and insufficient inspiration
  • 4. • Need to consider some specific features in children: Thymus CTR – exceed usual 50% Kink of trachea to right – If < full inspiration, tracheal kink to right. Soft tissues – prominent in children e.g. anterior axillary fold crossing chest wall can mimic pneumothorax.  Plaits of hair over upper chest mimic infiltrations. Pleural effusions – Seen as separation of lung from chest wall with relative preservation of CP angle and accentuation of lung fissures.
  • 5. Thymus • Normal thymus in children – widened mediastinum. • Lateral margin shows undulation – thymic wave. • Towrads right, normal thymus may show triangular “sail-like” configuration. • Decreased size at stress and with steroids. • Pathology identification can be difficult. • USG helps – cystic lesions from homogenous normal thymus. • MRI: Normal thymus homogenous SI while pathologies – heterogenous.
  • 6.
  • 7. • Fluoroscopy: Need to limit radiation exposure, pulsed rather than continuous. • Evaluation of differing radiolucencies in suspected foreign bodies. • Obstructive emphysema: affected lung shows little volume change with respiration, mediastinum shifts contralaterally on expiration. • Lateral fluoroscopy: for dynamic evaluation of tracheomalacia. • Barium swallow: Vascular rings, extrinsic masses, laryngeal clefts and TOF. • Either single contrast barium or water soluble contrast studies.
  • 8. MRI • Cardiac gated MR and MRA, assessment of cardiac lesions, great vessels, mediastinal masses, tracheobronchial anomalies and neurogenic masses.
  • 9. Ultrasonography: • Obviates the need for radiation. • Evaluation of pleural fluid, pleural masses, peri diaphragmatic masses and neck masses, pericardial disease, diaphragmatic pathologies, evaluation of thymus. • Antenatal ultrasonography – can identify the congenital pathologies like sequestration.
  • 10. • Bronchography: • HRCT (thin sections) almost eliminated bronchography in children. • Still used for functional bronchography and dynamics of tracheobronchomalacia. • Angiography: • Therapeutic in bronchial artery embolization. • In severe hemorrhage/ Hemoptysis in cystic fibrosis.
  • 11. CT Scan • Problems – Cardiac and respiratory motion artefact.  Less good tissue contrast due to paucity of mediastinal fat. Ultrafast electron beam CT , Spiral CT and volumetric CT used – reduce scan time  reduce need for sedation. • HRCT – Diffuse lung disease assessment. Opportunistic lung disease assessment. Road map for minimal invasive thoracic procedures.
  • 12. Tracheobronchial abnormalities Tracheal agenesis: • Rare. • Maternal polyhydramnios. • Respiratory distress, absent cry and cannot intubate. • 3 types: Type I: No upper trachea, lower trachea Oesophagus Type II: No trachea, common bronchus Oesophagus Type III: Separate bronchi, separately connected to oesophagus.
  • 13. Tracheal stenosis • Acquired or congenital (rare). • Following prolonged intubation or traumatic suctioning. • Congenital stenosis d/t complete cartilaginous ring. • Focal/generalized/funnel shaped. • Funnel shaped d/t pulmonary artery sling. • Presentation: 1st year of life with biphasic stridor. • Bronchoscopy, CT, MRI. • Associated anomalies: Tracheo-esophageal fistula, pulmonary agenesis or hypoplasia, pulmonary artery sling and bronchial stenosis.
  • 14. Tracheal stenosis. A, Axial CT shows severe narrowing of the trachea at the level of thoracic inlet (arrow) approximately 7 cm from the glottis. B, Coronal MiniP image shows severe narrowing (arrow) at the level of thoracic inlet.
  • 15. Tracheomalacia • Expiratory collapse of trachea due to softening of tracheal wall. • Secondary to: Cartilagenous anomalies. Tracheostomy. Oesophageal atresia or TOF. Chronic inflammation (cystic fibrosis, recurrent aspiration, immunodeficiency). Extrinsic compression (vascular rings, slings or aberrancy). Neoplasia.
  • 16. • Expiratory wheeze, exacerbated with crying, normal at rest. • Lateral fluoroscopy: Exaggerated decrease in sagittal width of trachea during expiration. • Dynamic CT: assess cross sectional anatomy and compliance of trachea. Tracheomalacia. Radiograph of the trachea in a 2-month-old infant with stridor shows marked diffuse tracheal narrowing during expiration (arrows). Radiographs of a 3-week-old infant with Hurler disease
  • 17. Tracheo-oesophageal fistula • Choking, cyanosis, coughing at feeding, insidiously as chronic respiratory infection. • Oesophageal atresia – obvious diagnosis. • Majority associated with oesophageal atresia. • If not, diagnosis difficult. • Contrast oesophagogram: Fine hair-like structure connecting oesophagus and trachea with linear opacification of posterior tracheal wall.
  • 18. • Type A - Esophageal atresia without fistula so-called pure esophageal atresia (10%) • Type B - Esophageal atresia with proximal TEF • Type C - Esophageal atresia with distal TEF (85%) • Type D - Esophageal atresia with proximal and distal TEFs • Type E - TEF without esophageal atresia or so-called H-type fistula (4%)
  • 19. Bronchial atresia • Upper lobe bronchi frequently atretic. • Newborn: Mass occupying part or all of an upper lobe (fetal lung fluid trapped behind the atresia). • Later, fetal lung fluid escapes via pores of kohn/canals of lambert – round opacity central to air trapping. • Associations: Bronchogenic cyst, intralobar sequestration or cystic adenomatoid malformation.
  • 20. Bronchial atresia. Axial CT shows an area of mucoid plugging in the left lower lobe (white arrow), and distal to this there is an area of hyperlucency (black arrow), consistent with bronchial atresia.
  • 21. Tracheal bronchus • also known as PIG bronchus. • 1% of normal population. • right upper lobe bronchus directly arises from the trachea.
  • 22. Tracheal bronchus. Coronal CT shows the tracheal bronchus (bronchus suis) (arrow) originating from the trachea and supplying the right upper lobe.
  • 23. Congenital pulmonary venolobar syndrome • Scimitar syndrome • Congenital aplasia or hypoplasia of one or more lobes of right lung. • Other variable features: Partial anomalous pulmonary venous return Anomalous or rudimentary arterial supply of the hypolplastic lobes (small pulmonary artery or supply directly from thoracic aorta/abdominal aorta/celiac axis). Hemidiaphragm abnormality Small hemithorax, obscuration of heart border, retrosternal soft tissue density.
  • 24. • AP view: Anomalous vein has “Turkish Scimitar” shape, drains into IVC or even hepatic vein or portal vein or right atrium. • May be association with pulmonary sequestration (right lower lobe) – appears as mass of abnormal lung tissue.
  • 25.
  • 26. Lung Agenesis • Small opaque hemithorax, ipsilateral mediastinal shift • Presentation: Neonatal respiratory distress. Can even present in adulthood, radiologically as “White- out” hemithorax. • Bronchography/Bronchoscopy: Absent mainstem bronchus • Angiography: No pulmonary or bronchial artery circulation. • Association: VATER syndrome • D/D: Pulmonary hypoplasia and complete lung atelectasis
  • 27. Pulmonary Hypoplasia • Factors compromising thoracic space available for lung growth. • Intrathoracic: diaphragmatic hernia or extralobar sequestration • Extrathoracic: Oligohydramnios/arthrogryphosis • Classically right lung involved. • Right sided obstructive heart disease • Association: Diaphragmatic hernia, renal agenesis/dysgenesis • Imaging: • Decrease in volume of right hemithorax. • I/L mediastinal shift. • Obscuration of heart border d/t extrapleural areolar tissue.
  • 28.
  • 29.
  • 30. Congenital Lobar Overinflation/emphysema • Progressive overdistension of a lobe or may be 2 lobes. • Emphysema – misnomer, no alveolar wall destruction. • Cause: Ball-valve mechanism obstruction of bronchus Abnormal bronchial cartilage deficiency/dysplasia Inflammatory changes Wall abnormality Inspissated mucus Mucosal folds/webs Intraluminal Broncial stenosis Extrinsic vascular or mass compression Extraluminal cause
  • 31. • M:F = 3:1 • Associated anomalies: Cardiovasular up to 50%, PDA, VSD and TOF • Lobar involvement: Upper lobes or right middle lobe • Left upper – 43%, Right middle – 32%, right upper – 20%, lower lobes – 5%. • Radiography: • Neonate: Fluid may get trapped, opaque enlarged hemithorax. • Later, fluid resorption, grossly overinflated lobe with generalized hypertransradiancy, marked attenuation of pulmonary vessels, compression of adjacent lobes.
  • 32. Congenital lobar emphysema/overinflation. Chest X-ray shows gross overinflation of the right lung which is hypovascular with marked shift of the mediastinum to the left and herniation of the lung into the left hemithorax (arrow). (B) CT of right middle lobe congenital lobar overinflation/emphysema causing shift of the mediastinum to the left with marked distortion of the pleural reflections to the left of the midline. Hyperexpansion of the left upper lobe with a portion herniated across the midline. There is shift of the mediastinum to the right, flattening of the left hemidiaphragm and some compression of the left lower lobe.
  • 33. Bronchopulmonary foregut malformations • Developmental anomalies from abnormal budding of the embryonic foregut and trachea-bronchial tree. Foregut cysts Bronchogenic cysts Enteric and neurenteric cysts Cystic hamartomatous adenomatoid malformation Pulmonary sequestration
  • 34. Bronchogenic cysts • ½ of all congenital thoracic cysts • Intrapulmonary or mediastinal (>common, earlier budding abnormality) • Lined by ciliated epithelium, may contain smooth muscle and cartilage • Mediastinal cysts: paratracheal (right sided >), carinal (m/c) or hilar • No communication with tracheobronchial tree • Instrumentation or infection – air-fluid level or air filled cyst. • D/D – Acquired cyst, cystic mesenchymal hamartoma.
  • 35. CT: Large fluid density lesion in right superior mediastinum, no invasion into mediastinum or lung Coronal T2-weighted image in the same patient shows a hyperintense lesion (arrow) splaying the carina.
  • 36. Enteric cysts • Early embryogenesis • Located in posterior mediastinum • If in oesophageal wall, oesophageal cysts or duplication cysts. • Can present early with acid secretion, may rupture into tracheobronchial tree leads to hemoptysis. • Large posterior mediastinal mass (right-sided). • Tc-MDP scan, uptake – gastric mucosa. Esophageal duplication cyst in a 3-year-old girl with cough and dyspnea. (a) Chest radiograph shows homogenous opacification of the right hemithorax (arrows) at the time of first admission. (b) Follow-up CT scan 3 years later shows a large cystic periesophageal mass (arrows)
  • 37. Neuroenteric cysts • Posterior mediastinal masses with associated vertebral abnormalities. • MRI needed to evaluate thoracic or spinal components of these cysts. • Foregut cysts can have water attenuation or even increased depending on viscousity of content. • CT attenuation or MRI intensity varies. • Usually unilocular and no enhancement.
  • 38. Neurenteric cyst in female patient with flank pain. (a) Chest radiograph shows a well-defined round mass (arrow) in the lower thoracic region. (b- c) Both axial T1-weighted – and coronal T2-weighted MR images show a large mass that is of homogenous high signal intensity in the right paravertebral region (arrow). The cyst presumably contains proteinaceous fluid. (d) The photograph of the resected tumor shows a thick-walled encapsulated cystic mass.
  • 39. Congenital Cystic Adenomatoid Malformation • Hamartomatous proliferation of terminal bronchioles at the expense of alveolar development. • Lesions composed of both cystic and solid components. • Cysts communicate with tracheobronchial tree. • Predilection for upper lobes. • Type I: m/c, 50%, variable cysts, at least 1 cyst > 2 cm d, < 5% congenital anomalies. • Type II: 41%, smaller, uniform cysts < 2 cm, 50% children anomalies (renal, intestinal, skeletal, cardiac) • Type III: microcysts, solid in gross, fetal hydrops and polyhydramnios, associated congenital anomalies, poor prognosis.
  • 40. Modified Stocker CPAM Type Description • 0 Incompatible with life • 1 Commonest type (>65%) Several large intercommunicating cysts (up to 10 cm) Mediastinal shift is common • 2 10–15% of cases Smaller than other types Small evenly sized cysts (up to 2 cm) Often associated with other congenital abnormalities • 3 ~8% of cases Large solid lesion with small cysts (1.5 cm) Nearly always causes mediastinal shift Poor prognosis • 4 10–15% of cases • Large cysts (up to 7 cm) ,May be associated with, or a precursor of pleuropulmonary blastoma
  • 41. Cystic adenomatoid malformation. A, Axial CT shows large cystic spaces filled partially with fluid in the medial aspect of the right upper lobe. B, Axial CT shows multiple small cystic lesions in the left lower lobe in type 2 CPAM. C, Coronal CT in same patient shows multiple small cystic lesions in the left lower lobe.
  • 42. Type I cyst: Multiple air filled cysts in left hemithorax, thin walled cysts, C/L mediastinal shift. CT: similar findings Chest X-ray: right cystic hamartomatous/adenomatous malformation type 1 with multiple cystic lesions in the right lower lobe showing air-fluid levels consistent with infection. (B) Axial CT scan through the lung bases show the thick-walled cysts in the right lower lobe.
  • 43. Pulmonary Sequestration • Congenital mass of aberrant pulmonary tissue that has no normal connection with the bronchial tree or with the pulmonary arteries. • Artery: usually anomalous, from aorta • Vein: Azygous system, pulmonary veins or IVC • Types: Intralobar and extralobar • Usually asymptomatic, m/c presentation is recurrent pneumonia.
  • 44. Imaging in sequestration • Identify sequestrated or dysplastic lung • Identify aberrant arterial or venous connections • Identify possible bronchial or gastrointestinal connections • Exclude other associated lung anomalies, horse-shoe lung or hypoplasia • Assess diaphragm integrity • Identify other associated anomalies
  • 45. Contd.. • Ultrasonography: Neonate – mass adjacent to liver or diaphragm • Antenatal USG: fetal chest mass with Doppler showing vascular connections to the sequestration. • CT: • Intralobar - Multicystic mass at lung bases • Extralobar – Soft tissue mass with avid contrast enhancement adjacent to diaphragm • MRI: Identification of pulmonary abnormality and vascular connections in multiplanar.
  • 46. Intralobar sequestration • >common, 70-85% • Within lung, no separate pleural covering, intimately connected to adjacent lung. • Venous drainage via pulmonary veins. • Location: lower lobes (98%), medial part of left lower lobe – m/c. • Anomalies <12%. • Diagnosis at adolescence with recurrent or refractory pneumonia.
  • 47. 2 round opacities overlying the left cardiac border. They have no silhouette with the left cardiac border, left diaphragm or descending aorta suggesting the left lower lobe location. Mass in the left lower lobe with soft tissue density (26 HU) , with defined border and peripheral calcification. No visceral pleura around the mass. No enhancement. arteries directly from aorta, vein drain into pulmonary v well defined wedge shaped echogenic lesion in right lower lung. D/D – CPAM III , separate feeding vessel from aorta
  • 48. Extralobar Sequestration • Less common, 15-25% • Extrapleural, can be intrathoracic or extrathoracic, almost always left lower lobe • Presentation- early, neonate with cyanosis, respiratory distress, infection • M:F = 4:1. • Venous drainage via systemic veins into right atrium • Separated from surrounding lung by own pleural covering. • Associations: 65% - Pulmonary hypoplasia, horse-shoe lung, CCAM, bronchogenic cysts, diaphragmatic hernia and CVS anomalies (TA and TAPVR).
  • 49. Left sided extralobar sequestration with a large systemic vessel from aorta, coronal CT shows, normal lung, beneath which left sided basal ELS and draing vein into azygous below diaphragm
  • 50. CHARACTERSTIC INTRALOBAR EXTRALOBAR Incidence More common ( 75 %) Less common( 25 %) Gender predisposition Equal Men 4: 1 Pleural investment Shares visceral pleura of parent lobe Separate visceral pleura Location Lower lobes(98%) , medial part of the left lobe Above, below or within diaphragm Venous Drainage Pulmonary venous Systemic venous (azygos, IVC, portal) Presentation Early adulthood with a history of pulmonary infection, chronic cough, or asthma. Asymptomatic mass (15%) Mostly present during first 6 months of life due to respiratory or feeding problems Radiographic Features Homogeneous consolidation with irregular margins or uniformly dense mass with smooth or lobulated contours. Single well defined, homogeneous, triangular shaped opacity in the lower thorax. May present else where in the thoracic cavity.
  • 51. DIAPHRAGMATIC ABNORMALITIES • Hernia • Eventeration • Agenesis • These anomalies associated with lung malformations and cause severe respiratory symptoms
  • 52. Bochdalek’s hernia • Through the posteropleuoperitoneal foramen. • Causes severe respiratory distress in the neonate . • Involves the left pleuroperitoneal foramen in 75 % of cases. • Neonatal radiograph shows a left-sided large intrathoracic mass of soft-tissue density • There is absence of the normal gas-containing bowel in the abdomen which is usually scaphoid on examination and other developmental abnormalities of the lung. • Prognosis depends on degree of underlying lung hypoplasia.
  • 53. The differential diagnoses are of other cystic-appearing intrathoracic masses in the newborn • Lobar emphysema, • Cystic adenomatoid malformations. • Sequestration, • Bronchogenic cysts
  • 54. 2 days old child showing a left-sided congenital diaphragmatic hernia with loops of bowel in the left hemithorax and shift of the heart and mediastinum to the right Lateral chest X-ray shows bulge in diaphragmatic contour just above posterior costophrenic recess. CT shows fatty mass abutting the defect in posteromedial aspect of left hemidiaphragm.
  • 55. Congenital eventeration of the diaphragm • Either partial or complete • Nearly always left sided, due to hypoplasia of the diaphragmatic muscle. • Most eventerations are minor, transitory, local diaphragmatic elevations found incidentally within the first few years of life Frontal and lateral chest x-ray shows smooth elevation of right hemidiaphragm medially and anteriorly consistent with an eventeration of the hemidiaphragm
  • 57. Immature lung disease • Small, premature infants with clinical, radiological and prognostic features differing from respiratory distress syndrome (RDS). • Birth weight < 1500 gms. • UNLIKE RDS, respiratory distress not seen until first 4-7 days. • Insufficient surfactant. • CXR: diffuse granularity of lungs, with relative absence of air bronchograms and little or no underaeration of lungs (unlike in RDS). • Complications: apnoea and bradycardia, persistent PDA • Need ventillatory support • Better prognosis compared to RDS (overall survival of 82%)
  • 58. Respiratory Distress Syndrome • Immaturity • <2.5 kgs, <36 weeks gestation • Leading cause of death in newborns • Symptoms shortly after birth, chest wall retraction, cyanosis, grunting • Deficiency of pulmonary surfactant. • hallmark features: reticular granularity of the lungs due to superimposition of multiple acinar nodules, related to atelectatic alveoli and diffuse pulmonary under aeration. • Air bronchograms due to coalescence of areas of atelectasis around dilated terminal bronchioles • Pulmonary interstitial emphysema: due to rupture of alveolar air sacs
  • 59. Hyaline membrane disease. (A) Mild changes aged 1 day-fine reticulonodular shadowing with prominent air bronchograms. (B) More advanced changes aged 3 days-marked pulmonary opacification with loss of diaphragmatic and cardiac contours.
  • 60. Pulmonary Interstitial Emphysema • also known as air block phenomenon. • almost always preceded by postitive pressure ventilation. • increase in transalveolar pressure leading to alveolar rupture ,dissection of air along peribronchial and perivascular spaces of interstitium. • tortuous linear luciencies of uniform size radiating from the hila through the lungs. • occurs in first week(CLD of prematurity usually in second week).
  • 61. Pulmonary interstitial emphysema. Fine reticular Shadowing in the right lung with deviation of the mediastinum contralaterally. RDSaffecting the left lung. Bilateral pneumothoraces in hyaline membrane disease. Right intercostal drain.
  • 62. Bronchopulmonary dysplasia or chronic lung disease of prematurity • Complication of ventilation in newborn. • Prolonged oxygen or ventilator therapy to developing lung. • 4 stages of progression: Stage I - ~ ARDS Stage II: 4-10 days, Bilateral “white-outs” (necrosis, epithelial repair with hyaline membrane, interstitial edema) Stage III: 10-20 days, Bubbly appearance of lung (alveolar overdistension) Stage IV: after 1 month, Classic bubbly appearance with alternating cyst like lucencies surrounded by curvilinear stranding of soft tissue.
  • 63. Bronchopulmonary dysplasia. Patchy shadowing from areas of loss of volume and fibrosis, with areas of compensatory emphysema, especially in the right upper lobe. Bilateral ill-defined reticulonodular markings, more prominent on the right, with obscuration of the right hemidiaphragm and heart border, positive air- bronchograms and hyperinflation of the left lower zone. No apparent atelectasis
  • 64. Bronchopulmonary dysplasia (BPD). A, Axial CT in a patient with BPD shows heterogeneous attenuation containing high attenuation and also areas of low attenuation. B, Axial CT shows bilateral multiple small cystic lesions in lungs of a patient with BPD.
  • 65. Transient tachypnea of newborn or wet lung disease • Delayed clearance and resorption of lung fluid. • Series of changes in X-ray: • First 6 hrs, fluid within lungs with increased vascular markings and hazy margins. • AT 10-12 hrs, gradual clearance, reticular granular densities ( ~ in RDS) but no underinflation of lungs. • At 48-72 hrs, gradual clearance from center to periphery.
  • 66. Meconium Aspiration Syndrome • Cause: intrauterine or intrapartum aspiration of meconium • Secondary to intra-uterine hypoxemia • Leads to bronchial obstruction and chemical pneumonitis. • Bilateral patchy asymmetrical areas of opacification with marked overinflation. • Complication: Pneumothorax and pneumomediastinum. • Radiological improvement lags behind clinical improvement. Meconium aspiration. There is marked overinflation of the lungs with coarse nodular shadowing secondary to meconium aspiration. Bilateral chest drains drain pneumothoraces
  • 67. Chest radiograph in a older child
  • 68. Pulmonary infections • Viral infections > bacterial • Air trapping or atelectasis > common in children < 8 yrs (small caliber peripheral airways, more collapsible and more mucus gland lining the airways) • Role of imaging: Confirm the presence, localization, extent and complication. • Not specific for specific organism.
  • 69. Tuberculosis • Primary TB causes localized air space disease (segmental or lobar) and regional node enlargement. • Occasionally, pleural effusion. • Caseation and necrosis of lymph node or inflammatory focus can occur (weeks later). • Resistance leads to involution or calcification . • Poor resistance or overwhelming infection, extension, larger area of lung involvement with effusion. • From lymphatic to venous system via thoracic duct leads to milliary nodules.
  • 70. 6 yr boy, presentation X-ray shows, tuberculoma right lower lung, f/u X-ray 4 yr later, parenchymal calcification with calcified nodes Interstitial granular densities distributed throughout the lungs, with relative basal and apical sparing. No pleural effusions. No loss of volume.
  • 71. Inhaled foreign body • May be radiopaque or non-radiopaque • Tend to enter right main bronchus • Complete obstruction – peripheral collapse • Incomplete obstruction – obstructive emphysema • Films in expiration or decubitus position and inspiration, if needed fluoroscopy, mediastinal shift away from obstructive emphysema on expiration/decubitus position (abnormal lung dependent). • If clinical suspicion (negative radiograph) – Bronchoscopy.
  • 72. Foreign body inhalation. (A) Obstructive emphysema from a foreign body in the left main bronchus. (B, C) Another child showing loss of volume in the left lung with patchy collapse in the apex of the left lower lobe; in inspiration (B) the mediastinum is slightly to the left; in expiration (C) the volume of the left lung changes little with the mediastinum swingi ng to the right.
  • 73. Cystic fibrosis • 2nd m/c chronic respiratory illness among children and young adults. • Chr 7, cystic fibrosis gene, Autosomal recessive. • Infants – atelectasis, focal or generalized overinflation with mucus plugging partially obstructing the airway. • Initial feature similar to viral pneumonitis. • Older children – overinflation, bronchial wall thickening, dilatation and mucus plugging – bronchiectasis. • Bronchiectatic cavities – air-fluid levels. • Hilar adenopathy, pulmonary hypertension.
  • 74. • HRCT – Early changes, hallmark – extensive central bronchiectasis. • Complication assessment: • Pneumothorax • Hemoptysis – source of bleeding identified by bronchial arteriography. • Cor-pulmonale and pulmonary hypertension.
  • 75. Bilateral predominantly upper lobes bronchiectasis​ with patchy consolidations and mild hyperinflation. Bilateral severe, widespread bronchiectasis with occasional mucus plugging and background mosaic attenuation, most likely due to air trapping. Lung volumes are increased.
  • 76. Cystic fibrosis. A, Coronal CT in a patient with cystic fibrosis shows extensive cystic bronchiectatic changes predominantly seen in the upper lobes, along with bronchial thickening. The lungs are hyperinflated. B, Axial CT in the same patient shows extensive bilateral upper lobe–predominant bronchiectatic changes along with bronchial thickening and areas of mucoid plugging.
  • 77. Idiopathic pulmonary haemosiderosis • Unknown aetiology. • Intra-alveolar hemorrhage. • Acute hemorrhage – bilateral hazy opacification ~ pulmonary edema • After blood clears up, hemosiderin deposited in lung septa – reticulonodular interstitial pattern. • Diagnosis: hemosiderin laden macrophages in sputum. Idiopathic pulmonary haemosiderosis. Perihilar shadowing with a reticulonodular pattern in the peripheral lung fields.
  • 78. Pulmonary alveolar proteinosis • Lipoprotenaceous deposits in alveolar spaces • M;F – 2:1, ~ 20 years of age. • CXR: multiple acinar nodules in miliary pattern, may coalesce, larger areas of consolidation. • CT: nodules more in dependent lung portions • Histology: PAS positive staining
  • 79. Fig. 9.25 (A) Pulmonary alveolar proteinosis. Chest X-ray showing diffuse alveolar shadowing in a perihilar distribution with some fine linear change in the upper zones. (B) High-resolution CT scan confirming these appearances showing diffuse alveolar exudate with interstitial thickening most marked in the non-dependent areas of the lung.
  • 80. References • Textbook of Radiology and Imaging, David Sutton. • RSNA articles Primary tuberculosis in childhood: radiographic manifestations. • Images from different web search.

Editor's Notes

  1. Differentiation between PA and AP fil difficult. Difficulties in imaging – motion artefact and insufficient inspiration For centring use anterior ribs ends over clavicle ends as clavicle ends are difficult to locate.
  2. Thymic wave sign correspond to indentations of ribs on inner surface of thoracic cage.
  3. HIGH SENSITIVITY THEN CONVENTIONAL XRAY DEMARCATE ANATOMY, CHEST AND PLEURAL LESION, MEDIASTINAL LESION , TRACHEA AND BRONCHI . MIP IMAGING FOR VASCULATURE AND SMALL NODULE ASSESMENT MINIIP QUANTIFICATION OF AAIR TRAPPING AND AIRWAY DISORDERS 3D VOLUME RENDERED FOR CARDIOVASCULAR ANATOMY.
  4. May be due to obstructive leion cartilaginious bar or vascular insult in intrauterine life. ANTENATAL USG – ECHOGENIC ENLARGED LUNG , PLEURAL EFFUSIONS MARKEDLY DILATED FLUID FILLED BRONCHI DECREASED CTR DUE TO INCREASED LUNG VOLUME AW CONGENITAL HEART DISEASE, RADIAL RAY ANAMOLIES AND DUODENAL ATRESIA. DIAGNOSIS – CAUTIOUS INJECTION OF WATER SOLUBLE CONTRAST TO ESOPHAGUS. DD LARYNGEAL ATRESIA SEVERE TRACHEAL STENOSIS.
  5. CT – O SHAPED TRACHEA. ECCENTRIC OR CONCENTRIC SOFT TISSUE THICKENING INTERNAL TO NORMAL APPEARING TRACHEAL CARTILAGE PROLONGED INTUBATION – PRESSURE NECROSIS MC OCCUR AT TRACHEOSTOMY STOMA OR AT LEVEL OF TUBE BALLON DIFFUSE TRACHEAL NARROWING AMYLOIDOSIS COPD WEGNERS TRACHEOMALACIA ULCERATIVE COLITIS RELAPSING POLYCHONDRITIS SARCOIDOSIS
  6. CF MOUNIER KUHN MARFAN EHLER DANLOS PLAIN XRAY NORMAL OR DILATED TRACHEA EXPIRATORY FILM IN LATERAL PROJECTION USEFUL CT DILATED TRACHEA WITH POSTERIOR BOWING OF MEMBRANOU PORTION OF TRACHEA DURING EXPIRATION –COLLAPSE GREATER THEN 70 PERCENT COLLAPSE OF TRACHEA IN EXPIRATIO IN CHILDREN SPECIFIC FOR DIAGNOSIS
  7. TREATMENT – SPLINTING OF MEMBRANOUS PORTION OF TRACHEA.
  8. MATERNAL POLYHYDROMNIOS INABILITY TO PASS NG TUBE CURLING OG NG PROXIMALLY EXCEPT IN H SAPED PRESENCE OF AIR IN STOMACHN IN THE PRESENCE OF ATRESIA DUR TO DISTAL FITUL ACQOURED MALIGNANCY RADIOTHERAPY TRAUMA CHRONIC INFLAMMATION POST TRACHEOSTOMY
  9. Bronchoceles with air fluid level may form radiating from hilum CT OBSTRUCTION VASCUARITY BRONCHOCELE , VASCULAR COMPONENT TO RULE OUT SEQUESTRATION.
  10. Anamolous pulmonary vein curving medially and inferior ly to diaphragmand progressively widening giving schimitar appearance.
  11. Coronal MIP image from ct scan show a large right pulmonary vein that is extending into the right lower lobe parallel to the right heart border and extending below diaphragm to drain into the IVC.
  12. AGENESIS – ABSENCE OF LUNG TISUE AND BRONCHI APLASIA – ABSENCE OF LUNG TISSUE WITH RUDIMENTARY BRONCHUS HYPOPLASIA- PRESENCE OF BOTH BRONCHI ND ALVEOLI IN UNDERDEVELOPED LOBE. RIGHT LUNG AGENESIS HAVE INCREASED MORTALITY DUE TO INCREASED CARDIOVASCULAR ANAMOLIES
  13. Pulmonary marings passing through it differentiate it from pneumothorax and pulmonary cysts Septa and vascular structures located in periphery of expanded air spaced whereas in Pulmonary interstitial emphysema they are in centre CPAM SOFT TISSUE PRESENT NOT PRESENT IN CONGENITAL LOBAR HYPERINFLATION.
  14. CPAM DONOT HAVE SYSTEMIC ARTERIAL SUPPLY SYSTEMIC RTERIAL SUPPLY MAY BE PRESENT IN SMALL CYSTIC CPAM KA HYBRID LEIONS
  15. Respiratory failure and pulmonary hypertension Posterolateral bochdhaleck 70-75 Anterior Morgagni 23-28 Central 2-7 percent
  16. Normal cxr after 6 hrs rule out RDS.
  17. RDS CLEARING FROM PERIPHERY TO CENTRE