1. Common Neonatal Chest Xrays
Lizette C. Sistoza, M.D.
Arrowhead Regional Medical Center
July 9, 2009

2. Normal Chest
The initial respiratory efforts of the newborn are rather exuberant and very adequately aerate the newborn infant’s lungs in most cases.
Negative pressures of 20-60cm of water are regularly generated, and tidal volumes of the first few breaths have been shown to be at least 2-3 times normal resting tidal volumes.

3. Normal chest
There is more pronounced effort on the newborn to accomplish initial inflation of the lungs.
While aeration still is a little uneven (some alveoli remain unexpanded or filled with fluid), most of the alveolar mass is aerated.

4. Normal chest
Hilar and parahilar regions are less prominent than in older infants and children. A normal air bronchogram is seen in the trachea and major bronchi. Slight right-sided deviation of the trachea is normal.

5. Normal chest
It is mandatory that chest examination be performed with adequate degrees of inspiration.
An underinflated chest can suggest serious cardiac or pulmonary disease

6. Normal chest: poor inspiration
Poor inspiration and rotation to the left produce an abnormal-appearing chest.
A few minutes later, deep inspiration results in a normal chest roentgenogram

7. Normal chest: lordotic position
In young infants, the upright posteroanterior view may appear as though the patient were purposely positioned for an apical lordotic view
In such cases, the cardiac apex may be so prominent suggesting a right ventricular hypertrophy

8. Normal chest: Poor tube position
With supine positioning of the patient, this (prominent cardiac apex) does not usually occur, but at the same time with improper positioning of the xray tube, there could be gross distortion of the thorax and its contents

9. Normal chest: Pleural fissure
Visualization of the various interlobar fissure in the newborn infant is common.
This probably reflects the “wet” state of the normal neonatal lung.
Fissure visualization drops rapidly after the neonatal period.

10. Normal chest: Tracheal deviation
Trachea is much more flexible and mobile than in the older child
On expiration, there is normal deviation of the trachea to the right
Due to: a) normal left aortic arch anchors the trachea and does not allow it to deviate to the left, and b) plunger effect of the thymus gland being pushed upward into the cervical inlet during expiration

11. Rotation of the chest: Pseudohyperluscent lung
Rotation of the chest to one side of the lung is the most common cause of apparent hyperlucency of one lung
The hyperlucent side usually corresponds to the side of the rotation
To determine if chest is rotated, check the ribs: Anteriorly the ribs will appear shorter, and posteriorly they will appear longer on the side to which the chest is rotated

12. Normal chest: Skin folds
Skin folds are the most common artifact seen in newborn infants’ xrays.
Especially common in premature infants and results from the folding of excessively redundant skin.
Often misinterpreted as pneumothorax

13. Normal chest: Skin folds
Line produced by a skin fold travels across, and outside, the chest or across the diaphragm into the abdomen
Lack of visualization of vascular markings lateral to the edge of the collapsed lung, and at the same time, this space should be very black
A zone of increased density is seen along the medial edge of a skin fold due to increased thickness of the skin.

14. Vertical skin fold versus pneumothorax
A. Skin fold. Vertical orientation of the skin fold. B. True pneumothorax. Near-vertical orientation of the edge of the compressed lung. No lung markings are seen lateral to the edge of the lung. In A, even though hyperlucency lateral to the skin fold is present, lung markings still are visible beyond the line of the skin fold.

15. Thymus gland
The normal thymus usually is visible and identifiable at birth and, in many infants, up to the age of 2-3 years.
Classic appearance: bilateral and smoothly outlines superior mediastinal fullness, blending almost imperceptibly with the cardiac silhouette

16. Normal thymus
A. Infant. Thymic silhouette blends almost imperceptible with the cardiac silhouette. B. Older child. Thymus is not evident. C. With a pneumomediastinum present, the thymic lobes are clearly outlined.

17. Normal thymus: varying configurations
A. Notch sign. Pronounced notch on the left. Both right and left thymic lobes are large but normal. Right thymic lobe blends with the heart, producing a psuedo-right atrial appearance. B. Sail sign. C. Lateral view demonstrates the slightly undulating lower edge of the thymus gland. D. Lateral view demonstrating inferior retrosternal extension of the thymus.

18. Normal thymus: pseudocardiomegaly. A
Normal thymus: pseudocardiomegaly. A. Supine positioning in an infant results in a round cardiothymic silhoutte. Cardiomegaly or a mass might be erroneously be suggested. B. Same patient with an upright film demonstrates a normal cardiothymic silhoutte.

19. Normal thymus: pseudopneumonia. A
Normal thymus: pseudopneumonia. A. With slight rotation to the right, a prominent right thymic lobe appears as a consolidating pneumonia of the right upper lobe. B. With proper positioning, the right thymic lobe now has a more typical appearance.

20. Transient tachypnea of the newborn (TTNB)
Appears soon after birth.
May be accompanied by chest restractions, expiratory grunting, or by cyanosis
Recovery usually is complete within 3 days
Radiologically, this syndrome frequently is termed wet lung disease. Also called retained lung fluid and respiratory distress syndrome type II

21. Transient tachypnea of the newborn (TTNB)
Increased incidence in infants delivered by cesarean section
Postulated that absence of squeezing of the thorax leads to retention of lung fluid
This fluid is subsequently cleared by way of the peribronchial lymphatics
Lymphatics overdistend, pulmonary compliance is altered, and respiratory distress develops

22. Transient tachypnea of the newborn (TTNB)
Fluid in the lungs of these infants consists primarily of fluid secreted by the fetal lung, but some amniotic fluid also is present
Respiratory distress usually becomes apparent 2-4 hours of age or even earlier
No alveolar diffusion block, but rather the problem is one of a “stiff” or “splinted” lung that does not ventilate properly until the fluid is cleared

23. Transient tachypnea of the newborn (TTNB)
Xray findings:
symmetrical parahilar radiating congestion
moderate to severe overaeration of the lungs
occasionally pleural effusions
Parahilar radiating pattern of congestion most often is misinterpreted for vascular congestion, meconium aspiration, or neonatal pneumonia
May also mimic xrays suggestive of cardiac failure and surfactant deficiency disorder

24. Retained fluid syndrome. A
Retained fluid syndrome. A. Pronounced, bilateral parahilar, radiating infiltrates and some fluid in the minor fissure. B. Lateral view shows overaeration, parahilar streaking, and fluid in the pleural fissures. C. Same infant 24 hours later demonstrates clearing or lungs with persistent little overaeration.

25. Surfactant deficiency Disease (SDD)
Hyaline membrane disease (HMD) or Respiratory Distress Syndrome (RDS)
Most common cause of respiratory distress in the preterm infant
Major problem rests with biochemical (surfactant deficiency) immaturity of the lungs, but it should also be remembered that there is also structural lung immaturity

26. Surfactant deficiency Disease (SDD)
Surfactant, a surface tension reducing lipoprotein, is produced by the alveolar cells and is essential for initial, and sustained, alveolar distention.
Its absence leads to an increased alveolar surface tension, decreased alveolar distensibility, and peristent collapse (atelectasis) of the alveoli

27. Surfactant deficiency Disease (SDD)
The infants cannot initially open, or thereafter normally inflate and aerate, their alveoli
Gas exchange becomes virtually impossible
Since the alveoli cannot be distended, these infants are unable to develop and maintain a significant functional residual volume
Intratracheal surfactant therapy has dramatically changed the spectrum of hyaline membrane disease

28. Surfactant deficiency Disease (SDD)
Histologically, the alveoli in SDD/HMD are uniformly collapsed, but the alveolar ducts and terminal bronchioles are variably distended
These latter structures are rimmed on their inner aspects by a layer of fibrin, the so-called “hyaline membrane” (believed to result from protein seepage from damaged capillaries but is not specific to the disease)

29. Surfactant deficiency Disease (SDD)
Classic roentgenographic findings:
pronounced pulmonary underaeration leading to small lung volumes
finely granular (ground-glass) appearance of the pulmonary parenchyma
peripherally extending air bronchograms

30. Surfactant deficiency disease: typical findings
Surfactant deficiency disease: typical findings. Lungs are underaerated and small for the overall size of the infant. Widespread peripheral air bronchograms and diffuse granularity of the lungs.

31. Surfactant deficiency disease: whiteout
Surfactant deficiency disease: whiteout. On the expiratory phase, the lungs become totally opaque with little, if any, air in the tracheobronchial tree.

32. Surfactant deficiency disease: basal changes in larger infant
Surfactant deficiency disease: basal changes in larger infant. The granularity of the lungs is seen primarily in the lung bases. In addition, the lungs are nearly normal in size.

33. Surfactant deficiency disease: clearing with surfactant therapy. A
Surfactant deficiency disease: clearing with surfactant therapy. A. Marked haziness/granularity of the lungs and air bronchograms. B. After surfactant therapy, the lungs are completely clear.

34. Leaky lung syndrome after treatment of SDD. A
Leaky lung syndrome after treatment of SDD. A. Hazy to granular lungs and air bronchorgrams. B. After surfactant, lungs are completely clear. C days later, the lungs become a little hazy representing early edema. D. A few days later, extensive opacity is seen. This is characteristic of the development of pulmonary edema of the leaky lung syndrome

35. Leaky lung syndrome (LLS)
Infants who require assisted ventilation therapy with high concentrations of oxygen, sustain damage to their pulmonary capillaries in the form of “oxygen toxicity” and associated hypoxia.
The end result is increased permeability of the capillaries, with leaking of fluid into the interstitium.

36. Leaky lung syndrome
At first, this fluid is interstitial, but eventually becomes both interstitial and intraalveolar.
Small premature infants even after demonstrating clear lungs after surfactant still have structurally immature lungs
They do not have enough alveoli and continue to have respiratory distress and require treatment with high flows of oxygen

37. Leaky lung syndrome
In combination with hypoxia, this leads to damage of the capillary basement membranes and leakage of fluid into the lung intersitium
LLS may also develop in low birth weight infants who have clear lungs from the onset.

38. Leaky lung syndrome
LLS often predisposes these infants to the development of the bubbly lungs of bronchopulmonary dysplasia (BPD) due to persistent respiratory distress requiring longer ventilator times with higher pressures.

39. Leaky lung syndrome. A. Initial severe SDD. B
Leaky lung syndrome. A. Initial severe SDD. B. Patient was refractory to surfactant and rapidly developed pulmonary edema. C. Clear lungs to LLS. Infant was born with clear lungs. Lungs however are still immature and have fewer alveoli. After 7-10 days, patient develops pulmonary edema. D. Lungs are hazy but reasonably large.

40. Amniotic fluid and meconium aspiration
Respiratory activity occurs in the fetus and it is not so exuberant that large volumes of amniotic fluid are aspirated into the lungs before birth
When intrauterine fetal distress occurs, these normally shallow fetal respirations become deeper and fetal gasping occurs
Fetal distress causes passage of
meconium in utero and thus not only
amniotic fluid is aspirated, but so is
meconium

41. Amniotic fluid and meconium aspiration
Infants with meconium aspiration usually are postmature, depressed, and in severe respiratory difficulty almost immediately after birth
Widespread airtrapping is the rule and results from the particles of meconium being lodged in the small peripheral bronchi
Complications include pneumomediastinum, pneumothorax and persistent pulmonary hypertension

42. Amniotic fluid and meconium aspiration – Chest xray findings
Vary with the degree of meconium aspiration and further influenced by the amount of amniotic fluid aspirated
In mild cases, findings may be normal

43. Amniotic fluid and meconium aspiration – CXR findings
In classic case of meconium aspiration
gross overaeration of the lungs and bilateral nodular infiltrates (represent areas of pathcy or focal alveolar atelectasis)
overaerated spaces in between
compensatory focal alveolar overdistention
In patients who recover, the roentgenographic clearing is slow, often taking days.

44. Amniotic fluid aspiration without significant meconium aspiration. A
Amniotic fluid aspiration without significant meconium aspiration. A. Diffuse nodular infiltrates and gross overaeration. B. 24 hours later, the lungs are completely clear.

45. Meconium aspiration. A. Typical fluffy, nodular infiltrates scattered throughout both lungs with overaeration B. Histologic material shows impaction of the terminal airways and alveoli with squames. C. A large fragment of meconium was in the right bronchus and caused obtructive emphysema with contralateral shift of the mediastinum and compression of the left lung.

46. Persistent Pulmonary Hypertension (PPHN)
Also called persistent fetal circulation (PFC)
Extraordinarily high pulmonary vascular resistance leading to right-to-left ductal shunting of blood.
Patients present with respiratory distress and cyanosis
Hypoxia is the cause of the problem inducing pulmonary arteriolar vasoconstriction and elevation of pulmonary artery pressures

47. PPHN Chest xray findings:
clear lungs
decreased pulmonary vascularity
right-sided cardiomegaly
Inhaled nitric oxide which leads to vasodilatation and improved oxygenation, has proved helpful in these patients.
Refractory patients may require ECMO therapy.

48. Pulmonary hypertension. Clear, hypovascularized lungs
Pulmonary hypertension. Clear, hypovascularized lungs. The heart is enlarged with a right-side pattern.

49. Neonatal pneumonia
Difficult to distinguish between patterns of bacterial and viral infections in neonates than in older infants and children
Bacterial infections still tend to be more alveolar and viral infections more interstitial

50. Neonatal pneumonia
Radiating parahilar streakiness and diffuse, hazy, or reticulonodular lungs favor viral disease
Coarse, patchy parenchymal infiltrates and consolidations favor bacterial disease
Pleural effusions are relatively common in bacterial infections

51. Neonatal pneumonia
Varies, but overall solitary lobar consolidations are uncommon
With group B streptococcus, findings mimic the granularity of the lungs seen in SDD; in some cases, more pronounced in the lung bases

52. Neonatal pneumonia: alveolar pattern. A
Neonatal pneumonia: alveolar pattern. A. Coarse nodularity throughout both lungs, more pronounced on right. Upper lobe is beginning to consolidate. Little fluid in the costophrenic angle. B. Bilateral hazy basal consolidations. C. Well-developed right upper lobe consolidation and one developing in the right lower lobe. Early similar changes in the left lower lobe. D. Opaque, totally opacified lungs in severe streptococcal pneumonia.

53. Neonatal pneumonia: interstitial pattern
Neonatal pneumonia: interstitial pattern. Diffuse reticulonodularity throughout both lungs. There is also diffuse underlying haziness.

54. Group B streptococcal pneumonia mimicking HMD. A
Group B streptococcal pneumonia mimicking HMD. A. Diffuse granularity throughout both lung fields indistinguishable from HMD. B. Another patient with hazy to granular lungs with parahilar streakiness. Also note pleural fluid bilaterally, more pronounced on the right.

55. Neonatal atelectasis
Segmental, lobar or even total atelectasis of a lung is not at all uncommon in the newborn
There is usually mechanical obstruction of a bronchus, either extrinsic (mass or vessel), or intrinsic (mucous or meconium plug).
Collapse is usually unilateral
The mediastinal structures often shift to the affected side

56. Lobar atelectasis. A. Typical appearance of a right upper lobe atelectasis. B. Peculiar but characteristic configuration of a right middle and lower lobe atelectasis. Diaphragmatic leaflet on the right is elevated.

57. Lobar atelectasis. C. Typical left lower lobe atelectasis. D
Lobar atelectasis. C. Typical left lower lobe atelectasis. D. Left upper lobe and lingular atelectasis. There is opacity of the left hemithorax and disappearance of the left side of the cardiac silhouette. Leftward and downward displacement of the mediastinum. There is compensatory overaeration of the right lung

58. Atelectasis due to improper endotracheal tube positioning
Atelectasis due to improper endotracheal tube positioning. Complete atelectasis of the left lung. The endotracheal tube is in the right bronchus.

59. Bronchopulmonary dysplasia (BPD)
Infants with BPD classically first suffered from SDD and thus were placed on oxygen and ventilator therapy
Oxygen toxicity leads to damage of the basement membrane of the pulmonary arterioles resulting in leakage of fluid into the pulmonary interstitium  edema and so called “leaky lung syndrome”

60. BPD
Infants then are subjected to prolonged ventilator-assisted therapy and its resultant barotrauma
End result is the superimposed development of the bubbly lungs of BPD
Note that not all these infants go on to develop BPD

61. BPD
Long-standing BPD is characterized by submucosal bronchial fibrosis, septal fibrosis, chronic inflammation, and squamous metaplasia.
Arteriolar changes reflecting the presence of hypertension also can be seen.

62. BPD Xray appearance of the bubbly lungs of BPD is quite variable
Findings depend on the size of the bubbles and the degree of associated insterstitial inflammatory change and fibrosis
Some may have large bubbles, while others show more interstitial scarring, fibrosis, and segmental atelectasis
Some will show overlap of BPD and LSS

63. BPD
In well-established BPD, the lungs are significantly injured, and healing takes up to 2 years
During the interval these infants suffer from hyperactive airways and susceptible to viral infections, especially RSV.
After 2 years, pulmonary function is mildly affected, but no serious sequelae have been documented.

64. A. Typical findings of SDD

65. B. Lungs clear with surfactant therapy

66. C. Early changes of pulmonary edema (leaky lung syndrome)

67. D. Superimposed bubbly changes of BPD

68. Pulmonary hemorrhage
Results from hypoxia and subsequent capillary damage
In massive pulmonary hemorrhage, the lungs appear somewhat homogeneously opaque and airless, and clinically, respiratory distres develops suddenly.
Blood may ooze from the nose, mouth, or endotracheal tube

69. Pulmonary hemorrhage
Etiology of massive hemorrhage is related to prematurity and severe hypoxia
Shunting through a patent ductus arteriosus with resultant high flow through the pulmonary circulation is also believed to contribute to pulmonary hemorrhage in some cases

70. Pulmomary hemorrhage. A
Pulmomary hemorrhage. A. This infant shows mild pulmonary edema as part of leaky lung syndrome. B. Abruptly, the lung findings change with marked increase in the size and opacity, characteristic of pulmonary hemorrhage.

71. Pneumothorax, Pneumomediastinum and Pulmonary Interstitial Emphysema
Manifestations of terminal airway or alveolar overdistention and subsequent rupture of these structures
This can occur with:
Infant’s own forceful, initial respiratory efforts
Positive pressure assisted ventilation
Widespread or focal air trapping

72. Pneumothorax, Pneumomediastinum and Interstitial Emphysema
When an alveolus or terminal airway ruptures, air escapes into the pulmonary intersititium and results in PIE.
Air then dissects along the bronchovascular sheaths to the outer periphery of the lung

73. Pneumothorax, Pneumomediastinum and Interstitial Emphysema
This air can decompress itself by passing directly into the mediastinum through the hilus of the lung (pneumomediastinum) or bursting through the visceral pleura into the pleural space (pneumothorax)
Development of PIE in a lung is a serious problem, for the lung is severely splinted – it does not ventilate and gas exchange cannot occur; pulmonary blood flow diminishes and aggravates the already compromised gas exchange.

74. Pneumothorax, Pneumomediastinum and Interstitial Emphysema
Meandering collections of tracking along the bronchovascular sheaths appear as tortuous air collections, radiating outward from the hilus of the lung
If positive pressure that induced them are not lowered, the air bubbles become more cystic
May also be replaced by large cystic pneumatocoeles
May also become localized to one lobe or one lung and result in an acquired form of lobar emphysema

75. PIE. A. Tortuous, meandering configuration of bubbles of air in the interstitium, radiating out from the hilum. B. Diagrammatic representation PIE

76. PIE: perivascular location. A
PIE: perivascular location. A. A target lesion is seen in the right midlung field. This represents air surrounding the bronchovascular complex. B. Histologic material showing air surrounding an arteriole. The target-lesion seen in A results from this type of air collection.

77. PIE: varying bubble formation. A. Bubbles are tortuous. B
PIE: varying bubble formation. A. Bubbles are tortuous. B. Much larger bubbles, which are now predominantly cyst-like

78. Pneumothorax, Pneumomediastinum and Interstitial Emphysema
When interstitial air reaches the pleural surface of the lung, subpleural blebs develop
When subpleural blebs burst, a pneumothorax develops
Large pneumothoraces can cause medial herniation of the pleural space across the anterior mediastinum
Lesser volume pneumothoraces are more difficult to identify

79. Pneumothorax: cloaking of the lung configuration. A
Pneumothorax: cloaking of the lung configuration. A. Bilateral pneumothoraces. B. Diagrammatic representation of the sites of free air collections: (1) over apex of the right lung, (2) over the anterior surface of the right diaphragmatic leaflet, (3)between the left lung and the heart, and (4) deep, over the posterior aspects of the diaphragmatic leaflets.

80. Pneumothorax. Larger pneumothoraces which are more easily visualized.

81. Medial pneumothorax. A. Large medial collection of free air between the left lung and heart. PIE is present in the right lung. B. Bilateral medial pneumothoraces produce a halo of free air around the heart. Some air is also present under the right lung.

82. Anterior pneumothorax: large hyperlucent hemithorax sign. A
Anterior pneumothorax: large hyperlucent hemithorax sign. A. Slightly large but very hyperlucent right hemithorax. The ipsilateral mediastinal edge is sharp. B. The left hemithorax is hyperlucent and the ipsilateral mediastinal edge very crisp. Thymus is compressed so as to produce a pseudomass.

83. Tension pneumothorax. Large, right tension pneumothorax with herniation of the pleural space across the mediastinum. The underlying ipsilateral lung is compressed.

84. Pneumomediastinum. Free air around the heart and great vessels, elevating both lobes of the thymus gland. Some air is also present along the inferior aspect of the heart.

85. Pneumomediastinum: angel wing configuration. A
Pneumomediastinum: angel wing configuration. A. Both thymic lobes are elevated by free mediastinal air beneath them. B. Large collection of air and more pronounced elevation of the thymic lobes. C. Thymic lobes are pushed into the apices of the thorax.

86. Pneumopericardium. Typical radiolucent halo of air surrounding the heart of a newborn infant with surfactant deficiency.

87. Congenital lobar emphysema
Some infants are asymptomatic, others present with severe neonatal respiratory distress
Physical examination reveals a hyperresonant hemithorax; breath sounds are diminished over the involved lung, and the cardiac apex is shifted away from the involved side

88. Congenital lobar emphysema
Most cases of CLE result from expiratory collapse of the bronchus secondary to segmental bronchial cartilage underdevelopment.
The loss of normal rigidity of the bronchus leads to redundancy and crinkling of the mucosa, and with the cartilage-deficient bronchial wall collapse, leads to a focal ball-valve mechanism of obstruction

89. Congenital lobar emphysema
Other causes of bronchial obstruction include congenital bronchial stenosis, intraluminal mucous plugs, obstructing mediastinal cysts or tumors, and vascular compressions.
On an acquired basis, also can occur in infants with BPD.

90. Congenital lobar emphysema Chest xray findings
Affected lobe is overdistended and the mediastinum shifted to the contralateral side
With upper lobe emphysema, secondary compression of the ipsilateral lower lobe is an important finding to look for.

91. Congenital lobar emphysema. A
Congenital lobar emphysema. A. Typical upper lobe emphysema with an overdistended left upper lobe and tell-tale atelectasis of the left lower lobe. Mediastinal shift to the right. B. Right upper lobe emphysema with more pronounced overdistention of the involved right lower lobe. C. Right middle lobe emphysema. Triangular radiolucency of the overinflated right middle lobe. Compressive atelectasis of the right upper and lower lobes.

92. Chylothorax
Etiology of chylothorax is uncertain, although most likely explanation lies in traumatic tear of the thoracic duct during delivery
Another possible explanation is that leakage occurs through congenital defects in the thoracic duct

93. Chylothorax Roentgenographic findings
opacification of one or the other side of the chest
contalateral shift of the mediastinum
In some cases, less fluid is seen and may collect along the base of the lung or around the mediastinum
In cases where entire hemithorax is opacified, ultrasound is the best and easiest way to confirm presence of pleural fluid

94. Bilateral hydro-chylothorax. A
Bilateral hydro-chylothorax. A. Extensive collection of fluid on both sides of the chest. The small, aerated lungs produce a radiolucent halo around the poorly visible heart. B. Post thoracentesis. Note the bilateral, small hypoplastic lungs. Bilateral pneumothoraces are present.

95. Pulmonary hypoplasia Cause can be classified in the following manner:
Extrathoracic fetal compression
Thoracic cage compression of the fetal lung
Intrathoracic fetal compression of the lungs
Primary pulmonary hypoplasia with no obvious cause of compression

96. Pulmonary hypoplasia Extrathoracic fetal compression
Best known cause is Potter’s syndrome
Renal agenesis leads to fetal anuria, maternal oligohydramnios, and subsequent compression of the fetal thorax and lungs by the uterus
This leads to impaired peripheral pulmonary parenchymal development

97. Hypoplastic lungs with oligohydramnios and polycystic kidneys
Hypoplastic lungs with oligohydramnios and polycystic kidneys. Grossly distended abdomen. Note small lungs and left pneumothorax. Presence of pneumomediastinum. Skinfold and small right pneumothorax.

98. Hyppoplastic lungs: oligohydramnios with leaking membranes
Hyppoplastic lungs: oligohydramnios with leaking membranes. Small thorax with severely hypoplastic lungs secondary to leaking membranes in utero. Also note deformed ribs.

99. Hypoplastic lung: chest wall dysfunction. A. Amyotonia congenita
Hypoplastic lung: chest wall dysfunction. A. Amyotonia congenita. Lung volumes are small and the diaphragm high in position. B. Baby with Down syndrome demonstrating small hypoplastic lungs and a bell-shaped chest.

100. Unilateral pulmonary hypoplasia
Unilateral pulmonary hypoplasia. Hypoplasia of the left lung is characterized by increased lucency and smallness of the lung. The vascularity is compensatorily increased in the right lung because the left pulmonary artery is also hypoplastic and cannot accept its normal volume of blood.

101. Diaphragmatic paralysis
Injury to the phrenic nerve with resultant elevation and fixation of a diaphragmatic leaflet can produce respiratory difficulty.
Paradoxical leaflet motion can be demonstrated with ultrasonography or fluoroscopy.
However, most times, paralysis is mild, paradoxical motion is not present, and symptoms are virtually absent.

102. Diaphragmatic paralysis. A. Elevated right diaphragmatic leaflet. B
Diaphragmatic paralysis. A. Elevated right diaphragmatic leaflet. B. Lateral view shows smoothly domed and elevated diaphragmatic leaflet. C. Ultrasound findings. Expiratory phase demonstrates both the right and left diaphragmatic leaflet to be high in position and at the same level. D. With inspiration, the left leaflet becomes flattened and moves downward while the right leaflet (arrow) remains domed and elevated. Right leaflet was paralyzed.

103. Eventration of the diaphragm
Can occur unilaterally or bilaterally.
A smooth bulge blending with the diaphragmatic leaflet is noted.
The abnormality represents a weakness in the diaphragm that allows herniation of the underlying organs.
Usually the condition is of no particular problem, but when very large or large and bilateral, can cause respiratory distress and surgical intervention may be required.

104. Diaphragmatic eventration. Elevated right diaphragmatic leaflet
Diaphragmatic eventration. Elevated right diaphragmatic leaflet. Patient also with scoliosis. Lateral view shows localized bulge of an eventration. Longitudinal US through liver demonstates the hump of the eventration.

105. Congenital diaphragmatic hernia
Classis xray appearance is one in which the left hemithorax is filled with cyst-like structures (loops of bowel), the mediastinum is shifted to the right, and the abdomen is relatively void of gas.
The abnormal positioning of the stomach is helpful in differentiating from cystic adenomatoid malformation (cysts are large that mimic bowel loops; stomach is normal in position and appearance).

106. Left diaphragmatic hernia. A
Left diaphragmatic hernia. A. Numerous loops of air-filled intestine and stomach is in the left hemithorax. Marked contralateral shift of the mediastinal structures. NGT in distal esophagus. B. With NGT now advanced into the stomach, stomach has been decompressed and the intestines partially decompressed. Much less mediastinal shift.

107. Right diaphragmatic hernia. A
Right diaphragmatic hernia. A. The liver and intestines have been displaced into the right hemithorax. The central, air-filled structure in the center is the stomach. There is pronounced shift of the mediastinum to the left. B. Another patient with right-sided hernia, not as massive as in A. Liver is still remains in the abdomen.

108. Points to remember: Know what is normal.
Recognize that improper positioning, rotation and poor inspiration in an xray may be misinterpreted as abnormal.
Recognize that certain respiratory disease processes mimic other respiratory problems (eg. HMD may look like pneumonia).
It is essential to correlate history and clinical picture with the roentgenograhic findings.

109. Thank you