This document provides information on interpreting chest x-rays in pediatrics. It discusses examining the entire x-ray using the "ABC" approach to systematically evaluate the abdomen, bones, and chest. Common respiratory conditions seen in children are described, including their etiology, pathology, clinical presentation, and key imaging findings. Conditions covered include asthma, atelectasis, bronchiolitis, bronchogenic cyst, croup, cystic fibrosis, and epiglottitis among others. The importance of careful evaluation for foreign body aspiration is also emphasized.

1. Chest X-Ray in
Pediatrics
Respiratory system disorders

2. Normal Chest
 Imaging Findings:
When interpreting a chest x-ray
in a child, the entire film should
be examined, not just the chest.
Use of the "ABC" approach
ensures that all areas of the film
are systematically examined.

3. A - Abdomen
A - Abdomen, check for:
bowel gas pattern suggesting
ileus or obstruction, free
intraperitoneal air, abnormal
calcification, abdominal situs,
diaphragm position.

4. B -Bones
B - Bone, check for:
fractures, lytic or
blastic lesions,
metabolic bone
diseases.

5. C - Chest
 C - Chest, check for: midline trachea
and mediastinum, abnormal
mediastinal and cardiac contours,
position of the aortic arch, pleural
effusions, pulmonary vascularity,
pneumomediastinum,
pneumothorax, pneumopericardium,
infiltrates, atelectasis.

6. In older infants and children,
a good inspiratory chest film
is one in which the
relationship of the 6th
anterior rib ends intersect
the domes of the diaphragm.

7. Normal Chest, Expiratory with
Tracheal Buckling
 Etiology/Pathophysiology:
Unexpanded alveoli cause decreased thoracic
volume.
 Pathology:
Collapsed alveoli causes the diffuse opacity in
the chest during expiration. The relative
fixation of the trachea at the thoracic inlet
while the distal trachea moves up and down
during inspiration and expiration causes
tracheal buckling during expiration.

8. Imaging Findings:

Normal Chest, Expiratory with
Tracheal Buckling
In older infants and children, a good
inspiratory chest film is one in which
the 6th anterior rib ends intersect the
domes of the diaphragm. Because the
volume of the thorax is decreased, one
sees increased pulmonary opacity,
pulmonary vasculature shadows
become confluent and prominent, and
heart and mediastinal contents
increase in size and prominence.

9. Normal Chest, Expiratory with
Tracheal Buckling
 In children less than 5 years old,
lateral buckling of the trachea at
or just above the thoracic inlet is
often seen during expiration.
This tracheal buckling occurs to
the side opposite the aortic arch,
usually to the right.

10. DDX: Normal Chest, Expiratory
with Tracheal Buckling
 Pneumonia
 Cardiomegaly
 Mediastinal mass
 Vascular congestion
 Congestive heart failure
 Pulmonary edema

11. Asthma
 Clinical Presentation:
Wheezing, labored breathing, irritative
cough with sputum.
 Etiology/Pathophysiology:
Edema of bronchial mucosa and
bronchospasm leads to decreased
bronchiole caliber which leads to air
trapping and hyperinflation. It is often
complicated by mucous plugging of the
bronchi causing atelectasis, most
commonly in the right middle lobe.

12. Asthma
Imaging Findings:

The chest is hyperinflated.
Transient subsegmental areas of
atelectasis may be present.
Pneumomediastinum may be
present, dissecting into the
subcutaneous tissues of the chest
and neck.

13. Atelectasis
Etiology/Pathophysiology:
Bronchial obstruction leading
to peripheral airway collapse
can be caused by mucous
obstructing the airway in
asthma or post-operatively,
or following aspiration of a
foreign body.

14. Atelectasis
Imaging Findings:

Atelectasis is associated with a shift of the
adjacent structures, such as the
mediastinum, into the involved
hemithorax. A "silhouette sign" occurs
when the collapsed lung abuts against the
heart and obliterates the margin between
the lung and the heart.

15. Bronchiolitis
 Clinical Presentation:
Respiratory distress in a child less than 18
months old.
 Etiology/Pathophysiology:
Acute viral respiratory illness leads to
edema and infiltration of bronchial walls
which leads to inflammatory obstruction of
small peripheral pulmonary airways.
Mucous plugging also contributes to small
airway obstruction.

16. Bronchiolitis
Etiology/Pathophysiology:
 The infant airway has several features
which distinguish it from the adult airway
and help to increase the susceptibility to an
effect of inflammatory bronchiolar
narrowing in infancy:
it is easily plugged by mucous or
inflammatory debris, the collateral
pathways of ventilation - pores of Cohn and
Lambert - are less well developed, it has
more mucous glands in the airways, and
the airways are more collapsible in
response to airway pressure changes.

17. Bronchiolitis
 Pathology:
Edema and inflammatory
infiltration of the bronchial walls.
 Imaging Findings:
The chest is hyperinflated. There
is peribronchial cuffing and
overdistended airways. Overtime
focal segmental/subsegmental
atelectasis may be seen.

18. Bronchogenic Cyst
 Clinical Presentation:
Mediastinal cysts in small
children can cause dysphagia or
respiratory distress due to
displacement of the esophagus
and / or trachea. Pulmonary
cysts are usually asymptomatic.

19. Bronchogenic Cyst
 Etiology/Pathophysiology:
Due to abnormal branching or budding
of the tracheobronchial tree.
Bronchogenic cyst is in the broad
category of bronchopulmonary foregut
malformations which makes them
related to enteric duplication cysts and
pulmonary sequestration.

20. Bronchogenic Cyst
Pathology:
Thin walled cysts lined by
respiratory epithelium. The
walls may contain mucous
glands, cartilage, elastic
tissue and muscle.

21. Bronchogenic Cyst
 Imaging Findings:
Occur in the mediastinum and lung with
equal frequency. Mediastinal cysts are
usually solitary, with 50% in the posterior
mediastinum, and 35% in the middle
mediastinum. Mediastinal cysts rarely
communicate with the tracheal tree and
are oval and rounded in appearance and
may change in shape with
inspiration/expiration.

22. Bronchogenic Cyst
 Mediastinal cysts are located either
centrally or in the
perihilar/subcarinal areas.
Pulmonary cysts are solitary, round
mass lesions located in the medial
third of the lung and don't
communicate with the
tracheobronchial tree until they
become infected.

23. Choanal Atresia
Clinical Presentation:
If unilateral, the patient
may be asymptomatic. If
bilateral, the symptoms
include dypsnea and
apnea during feeding.

24. Choanal Atresia
 Etiology/Pathophysiology:
Due to a membranous or bony
occlusion (septum) between the nose
and pharynx, associated with medially
bowing of the lateral walls of the nasal
cavity.
 Part of the CHARGE association -
coloboma, heart disease, choanal
atresia, retarted growth, genital
hypoplasia, and ear anomalies.

25. Choanal Atresia
 Imaging Findings:
On computed tomography, a
bony occlusion between the nose
and the pharynx can be
visualized.The lateral walls of
the nasal cavity are thickened
and bowed medially, and the
vomer is usually enlarged.

26. Croup (Acute
Laryngotracheobronchitis)
Clinical Presentation:
Inspiratory stridor with a
harsh cough and
hoarseness. The incidence
peaks in the second year
of life.

27. Croup (Acute
Laryngotracheobronchitis)
 Etiology/Pathophysiology:
Nearly always viral in origin. The
viral infection causes
inflammation and narrowing of
the subglottic airway causing
obstruction of the subglottic
airway and the larynx.

28. Croup (Acute
Laryngotracheobronchitis)
 Imaging Findings:
An AP film shows proximal subglottic
airway narrowing which is visible as
the "steeple sign" where there is loss
of the shoulder like subglottic trachea.
A lateral film of the airway should
always be taken to rule out the other
diseases in the differential of
inspiratory stridor, particularly
epiglottitis.

29. Croup (Acute
Laryngotracheobronchitis) DDX
Congenital subglottic stenosis
Subglottic hemangioma
Airway foreign body
Esophageal foreign body
Epiglottitis - 25% of epiglottitis
patient have subglottic airway
narrowing

30. Cystic Fibrosis (CF)
 Clinical Presentation:
Major manifestations are chronic
obstructive pulmonary disease,
pancreatic insufficiency with
malabsorption, and elevated sweat
electrolytes. It is the most common
lethal genetic disease in whites with
90% percent of the mortality due to
pulmonary infections.

31. Cystic Fibrosis (CF)
 Etiology/Pathophysiology:
Due to an inborn error of
metabolism causing dysfunction
of all exocrine glands leading to
thickened exocrine gland
secretions. The lungs are normal
at birth but become
progressively obstructed leading
to hyperinflation

32. Cystic Fibrosis (CF)
 . The thickened mucus in the airways
gives the patient a predisposition to
infection, often with Pseudomonas,
which over time results in bronchiectasis.
Eventually as the pulmonary disease
worsens the patient gets pulmonary
hypertension and cor pulmonale.
Pneumothorax and pulmonary
hemorrhage are common complications.

33. Cystic Fibrosis (CF)
 Imaging Findings:
The classical CXR signs are
hyperinflation, peribronchial
thickening, cystic bronchiectasis,
fibrosis, and scattered areas of mucoid
impaction. The cardiac silhouette is
normally narrowed due to the
pulmonary hypertension and the
generalized obstructive emphysema.

34. Diaphragmatic Eventration
 Clinical Presentation:
Usually are asymptomatic or have mild
respiratory distress.
 Etiology/Pathophysiology:
Abnormal elevation of the diaphragm due to
absent or deficient diaphragm muscles with
only the peripheral thoracic attachments
showing normal muscle. There are two types:
(1) congenital, due to defective diaphragm
muscle formation and (2) acquired, due to
atrophy of diaphragm muscles secondary to
prenatal or postnatal phrenic nerve injury. The
acquired type is the most common.

35. Diaphragmatic Eventration
 Pathology:
Marked decrease in muscle fibers between
the parietal pleura and the peritoneum. The
affected area appears membranous.
 Imaging Findings:
Generalized elevation of the diaphragm with
the abdominal viscera contained by a thin
but intact diaphragm.
 DDX:
 Anteromedial (Morgagni) hernia

37.  Рентгенонегативное контрастирование
воздухом применяют почти исключительно при
лечебно-диагностической
пневмоирригографии у детей с подозрением на
кишечную инвагинацию. В последние годы по
мере внедрения в клиническую практику
новых методов визуализации (компьютерная
томография, магнитно-резонансная
томография) многие исследования с
использованием рентгенонегативного
контрастирования уже не применяются
(пневмомедиастинография,
ретропневмоперитонеум и пр.).

38.  а - контрастное вещество (бариевая взвесь)
введено перорально, контрастирован желудок и
кишечные петли, расположенные в правом
гемитораксе - истинная правосторонняя
диафрагмальная грыжа у ребенка 2 лет;
 б - фистулография: контрастный препарат
(урографин) введен в свищевой ход у ребенка 13
лет с хроническим посттравматическим
остеомиелитом большеберцовой кости; в -
цистография: контрастный препарат (урографин)
по катетеру введен в мочевой пузырь,
определяется пузырно-мочеточниковый рефлюкс 4
степени с обеих сторон, нейрогенный мочевой
пузырь у ребенка 2 лет

39. Epiglottitis
 Clinical Presentation:
Seen in an older age group than croup,
usually around 3-10 years old. Presents
with drooling, fever, signs of systemic
toxicity, severe sore throat, rapidly
progressive dysphagia, inspiratory stridor,
and respiratory distress. Physical exam
shows a red, swollen, cherrylike tip of the
inflamed epiglottis. Note that both
epiglottitis and croup have inspiratory
stridor.

40. Epiglottitis
 Etiology/Pathophysiology:
The most common cause is bacterial
infection due to Haemophilus
influenza. Other less common causes
are angioneurotic edema, thermal
injuries from smoke inhalation, caustic
ingestion, hemorrhage, and radiation.
The enlarged aryepiglottic folds
account for much of the airway
obstruction

41. Epiglottitis
Imaging Findings:
 Careful radiographic evaluation is
essential. Personnel skilled in the
management of pediatric airway
obstruction and equipment for
emergency intubation must
accompany the patient to the
radiology department. The lateral film
should be done upright with no
attempt made to hyperextend the
neck which can cause complete airway
obstruction.

42. Epiglottitis
Imaging Findings:
 The lateral film shows a domelike
enlargement of the epiglottis with
thickened aryepiglottic folds,
supraglottic airway narrowing, and
obstruction. Twenty-five percent
have subglottic airway narrowing.
On the CXR lung volumes are
normal.

43. Foreign Body, Trachea
 Clinical Presentation:
The presentation varies, depending on
the size of the foreign body. There can
be sudden choking with acute
respiratory distress, or there can be
delayed symptoms with cough,
wheezing, and hemoptysis. Less
commonly the patient can present
with recurrent pneumonias.

44. Foreign Body, Trachea
 Etiology/Pathophysiology:
An aspirated foreign body causes a
spectrum of airway obstruction,
depending on its size and how long it
has been present. When the foreign
body is much smaller than the airway
you have a bypass valve effect giving
you normal aeration - air gets in and
out on inspiration and expiration.

45. Foreign Body, Trachea
 When the foreign body is only a little
bit smaller than the airway you have
a check valve effect giving you air
trapping - air gets in during
inspiration but does not get out on
expiration.
 When the foreign body is as large as
the airway you have a stop valve
effect - air does not get in or out
during inspiration or expiration.

46. Foreign Body, Trachea
DDX:
Congenital lobar
emphysema
Congenital pulmonary
airway malformation

47. а - свернутый зонд (стрелки) в оральном конце пищевода у новорожденного с атрезией пищевода;
б - дренаж (стрелки) в плевральной полости у младенца с напряженным пневмотораксом справа; круглые тени - электроды
от монитора; в - исследование по Вангестину: на коже промежности в проекции анального отверстия нанесена
рентгеноконтрастная метка (стрелка); по рентгеновскому снимку, выполненному в положении младенца вниз головой, опре-
деляется расстояние от метки до пузыря воздуха в атрезированной

48. Pneumonia, Bacterial
 Clinical Presentation:
Presents with an abrupt onset of
fever and tachypnea.
 Etiology/Pathophysiology:
Common pathogens include
Staphylococcus, Pneumococcus
(Streptococcus pneumonia), and
Haemophilus influenza. Bacterial
pneumonia usually has primarily
alveolar involvement without airway
involvement

49. Pneumonia, Bacterial
Pneumatoceles may form
during the recuperative phase
and are transient
accumulations of interstitial
air that have escaped through
necrotic bronchial foci and are
usually of little significance,
resolving over time.

50. Pneumonia, Bacterial
 Imaging Findings:
Homogeneous consolidation of all or
part of a lobe with air bronchograms.
Lung volume is preserved. Bacterial
infections are usually in the periphery
of the lung while viral infections are
more commonly in the center of the
lung in a perihilar location. Effusions
are often seen with bacterial
pneumonia.

51. Pneumonia, Mycoplasma
 Clinical Presentation:
Seen in late childhood or early adult
life. Presents with chest pain, cough,
mild chills, fever, and myalgia.
Probably is seen in younger children
but is asymptomatic or has very mild
symptoms.
 Etiology/Pathophysiology:
Mycoplasma pneumoniae is the
causitive agent.

52. Pneumonia, Mycoplasma
Imaging Findings:
See subsegmental or
segmental consolidation
which can involve the upper
and lower lobes and be
unilateral or bilateral. No air
bronchograms are seen, and
there can be small effusions.

53. Pneumonia, Pneumocystis Carinii
 Clinical Presentation:
Respiratory distress in an immune
compromised patient due to a
congenital immune disorder,
immunosupression treatment, or
AIDS.
 Etiology/Pathophysiology:
Pneumocystis Carinii, which is a
protozoa.

54. Pneumonia, Pneumocystis Carinii
 Imaging Findings:
The appearance is extremely variable.
The classical appearance is diffuse
bilateral central consolidation radiating
into the peripheral lung zones with
sparing of the apices. A patchy reticular
granular density that progresses rapidly
to diffuse alveolar consolidation is a
typical course. Effusion and
lymphadenopathy are rarely seen. The
CXR clears very slowly.

55. Pneumonia, Pneumocystis Carinii
 DDX:
Infections in Immune Suppressed
Hosts
 Viruses
 Bacteria
 Opportunistic organisms
◦Fungi - aspergillus, mucormycosis,
Candida, Nocardia
◦Protozoa - Pneumocystis carinii

56. Pneumonia, Round
 Clinical Presentation:
Most common in infancy and early
childhood.
 Etiology/Pathophysiology:
Caused by a bacterial infection.
 Imaging Findings:
Well circumscribed, rounded mass lesion in
a peripheral location with air bronchograms.
 DDX:
 Intrathoracic mass lesions - will not have air
bronchograms.

57. Pneumonia, Viral
 Clinical Presentation:
Respiratory distress.
 Etiology/Pathophysiology:
Respiratory syncitial virus is the most
common cause in early life. Other causes
include parainfluenza, adenovirus, and
influenza viruses. Inflammation begins in
the respiratory mucosa of the major bronchi
and spreads transmurally and
endobronchially into the adjacent
interstitium as well as into the peripheral air
spaces.

58. Pneumonia, Viral
 Imaging Findings:
Usually central in location. Hilar and
vascular radiographic sharpness is
lost due to bronchial wall thickening
with peribronchial interstitial edema
and inflammatory infiltrate. Due to
the central airway involvement there
is peripheral air trapping and
hyperinflation. Patchy pulmonary
densities can be seen and are usually
due to subsegmental atelectasis.

59. Pneumothorax, Spontaneous
 Clinical Presentation:
Sudden onset of pleuritic chest pain in a
teen with associated respiratory distress.
 Etiology/Pathophysiology:
Pneumothorax may occur in an otherwise
normal lung during normal respiration or
more commonly during episodes of cough,
resuscitation, or artifical ventilation.
 Imaging Findings:
A pleural line is demonstrated better on
the expiratory film than on the inspiratory
film.

60. Pulmonary Agenesis
 Clinical Presentation:
Unilateral agenesis is usually asymptomatic.
The child usually develops respiratory
distress and presents in the first year of life
when the remaining lung is compromised,
usually by a lower respiratory tract
infection.
 Sixty percent have other congenital
anomalies including cardiac lesions,
bronchogenic cysts, diaphragmatic hernias,
and skeletal anomalies (commonly vertebral
or rib anomalies).
 Agenesis of the right lung is associated with
a higher frequency of anomalies than
agenesis of the left lung.

61. Pulmonary Agenesis
 Etiology/Pathophysiology:
Due to complete failure of development of
one or both of the lung buds.
 Imaging Findings:
Asymmetry in chest volume and
configuration with overexpansion of the
normal lung often causing some
mediastinal shift to the contralateral side.
The definitive diagnosis is made via
pulmonary angiography which shows the
pulmonary artery to the affected side to be
absent.

62. Pulmonary Edema, Non Cardiogenic
[Drowning]
 Clinical Presentation:
The third highest cause of accidental death in
children.
 Etiology/Pathophysiology:
Causes include drowning, acute
glomerulonephritis, fluid overload, aspiration,
inhalation injury, neurogenic pulmonary edema,
allergic reaction, and adult respiratory distress
syndrome. It is due to injury of the alveolar
septa, increased permeability of the pulmonary
vascular endothelium, pulmonary microvascular
platelet aggregation, and finally intraalveolar
edema.

63. Pulmonary Edema, Non
Cardiogenic [Drowning]
 In drowning, the extent and severity
of the edema depends on the amount
of water aspirated and the degree of
hypoxia. Whether the water is fresh or
salt makes no difference on the
pulmonary findings.
 Imaging Findings:
One of three patterns is seen: a
normal chest, bilateral perihilar
pulmonary edema, or generalized
pulmonary edema.

64. Tuberculosis, Primary
 Clinical Presentation:
Cough and fever.
 Etiology/Pathophysiology:
The initial infection with the bacterium
Mycobacterium Tuberculosis is acquired via an
airborne route. If the initial infection is not
walled off, it may spread via bronchogenic
spread with multiple pulmonary foci, lymphatic
spread to more distant lymph nodes and
hematogenous (miliary) spread to kidneys,
lungs, liver, and meninges.
 Pathology:
The classic finding is caseating necrosis.

65. Tuberculosis, Primary
 Imaging Findings:
The initial focus has localized air space
consolidation and then spreads from the
periphery via lymphatic channels to regional
lymph nodes where the lymph nodes
enlarge after several weeks. If the infection
involutes the lesion can calcify with the
Ghon focus being the calcified peripheral
lung focus and the Ranke complex being the
calcified peripheral lung focus and the
calcified central lymph nodes.

66. Tuberculosis, Primary
 If resistance fails to develop and there is no
involution the initial peripheral focus can
extend to occupy an entire segment or lobe.
Often there may be an associated pleural
effusion. Primary TB has its peripheral foci
scattered throughout the lung fields.
Secondary, or reinfection, TB has 90% of its
lesions in apices. The lungs may take 4
years to clear after therapy. The classic
picture of primary TB is air space disease
associated with hilar/mediastinal
adenopathy and pleural effusion.

67. Tuberculosis, Miliary
 Clinical Presentation:
More common in younger children than in
older children.
 Etiology/Pathophysiology:
Hematogenous spread of tubercle bacilli
throughout the body, usually in the first few
months after a primary infection. The
younger the infant the more rapidly the
inflammatory process evolves.
 Pathology:
Granulomas.

68. Tuberculosis, Miliary
 Imaging Findings:
May take several days to show up on CXR.
Tiny, miliary densities are seen in the lungs
that represent a confluence of several
pulmonary granulomas. Hilar and
paratracheal adenopathy may also seen.
 DDX:
 Hematogenous spread of viral and fungal
infections
 Sarcoid
 Lymphoproliferative malignant disease

69. Diaphragm Rupture, Traumatic
 Clinical Presentation:
Upper abdominal tenderness, rigidity and
rebound tenderness after blunt or crushing or
penetrating injuries. Chest pain, dyspnea, and
hypertension may also be present.
 Etiology/Pathophysiology:
Due to blunt or crushing abdominal injuries
from sudden deceleration in a motor vehicle
accident, or more rarely stab and gunshot
wounds.
 Imaging Findings:
See abdominal contents such as bowel or solid
viscera in the chest. Can be confirmed by
passing a nasogastric tube or performing an
upper GI exam.

70. Pectus Carinatum
 Clinical Presentation:
Asymptomatic as it rarely causes
physiologic compromise of the lungs.
 Etiology/Pathophysiology:
Ventral protrusion of the upper portion of
the sternum and its costal cartilages with
bilateral flattening of the lateral chest wall.
 Imaging Findings:
The elevated protrusion of the upper
sternum is easily seen on the lateral chest
film.

71. Pectus Excavatum
 Clinical Presentation:
Asymptomatic as it rarely causes physiologic
compromise of the lungs.
 Etiology/Pathophysiology:
The lower part of the sternum and its costal
cartilages are partially rotated to the right and
depressed causing displacement of the heart to
the left.
 Imaging Findings:
On the AP film there is some deviation of the
heart to the left causing the right hilus and
bronchovascular markings to appear
prominent. The depressed body of the lower
sternum is easily seen on the lateral chest film.

72. Source
 Michael P. D'Alessandro, M.D.
 Peer Review Status: Internally Peer
Reviewed
 https://www.virtualpediatrichospital.org/p
roviders/PAP/ChestDiseases/ChestDisInde
x.shtml
