Pediatrics: Chest Flashcards
1
Q
How can you tell if a neonatal chest is hyper inflated or not?
A
Count the ribs:
More than 6 anterior or 8 posterior ribs above the diaphragm is too many (hyperinflated)
Note: Also look for flattening of the diaphragm or increased lucency under the heart.
2
Q
What is the best way to identify a pleural effusion on a neonatal chest radiograph?
A
Look for thickening of the minor fissure, then confirm by scrutinizing the costophrenic angle
3
Q
Hyperinflation and perihilar streaks on a neonatal chest radiograph…
A
Think MNoP
- Meconium
- Non-group B strep neonatal pneumonia
- asPiration
4
Q
Diffuse granular opacities with normal/decreased lung volumes on a neonatal chest radiograph…
A
- Surfactant deficiency disease
- Group B strep neonatal pneumonia
5
Q
Hyperinflation with ropy appearance of asymmetric lung densities in a term infant…
A
Think meconium aspiration
6
Q
Meconium aspiration is more common in…
A
Term or post-term infants
7
Q
What should you look for if you’re suspecting meconium aspiration…
A
Pneumothorax (present in 20-40% of cases)
8
Q
Classic findings of meconium aspiration
A
- Asymmetric rope-like pulmonary hyper densities
- Hyperinflation
- Pneumothorax (20-40% of cases)
Note: Usually in a term or post-term infant.
9
Q
Meconium aspiration is usually associated with under inflation/hyperinflation
A
Hyperinflation (due to ball-valve effect from obstructing aspirated meconium)
10
Q
Newborn with history of cesarean deliver with respiratory distress and bilateral coarse interstitial markings and fluid in the fissures that resolve by day 3 of life…
A
Transient tachypnea of the newborn
11
Q
Risk factors for transient tachypnea of the newborn
A
- Cesarean section
- Maternal sedation
- Maternal diabetes
12
Q
What is the time course of transient tachypnea of the newborn?
A
Peaks at day 1 of life and resolved by day 3
13
Q
What is the most common cause of death in premature infants?
A
Surfactant deficiency disease (AKA respiratory distress syndrome)
14
Q
Premature infant with respiratory distress and low lung volumes with bilateral granular opacities on radiography…
A
Think surfactant-deficiency disease
15
Q
How can you differentiate surfactant-deficiency disease from group-B hemolytic neonatal pneumonia…
A
Surfactant-deficiency disease will not cause pleural effusions (which are common in group-B hemolytic neonatal pneumonia)
16
Q
True or false: A normal plain film at 6 hours of life excludes surfactant-deficiency disease
A
True
17
Q
Central bleb-like lucencies in an infant being treated for surfactant-deficiency disease…
A
Normal treatment response
Note: Do not confuse this with pulmonary interstitial emphysema.
18
Q
Infants being treated for surfactant-deficiency disease are at an increased risk for…
A
- Pulmonary hemorrhage
- Patent ductus arteriosus
19
Q
What is the most common type of pneumonia in newborns?
A
Group-B beta-hemolytic strep pneumonia (acquired during vaginal birth)
20
Q
Bilateral granular opacities with low lung volumes in a newborn…
A
- Surfactant-deficiency disease (if premature)
- Group-B strep pneumonia (if pleural effusions are also present)
21
Q
Does neonatal pneumonia usually have increased or decreased lung volumes?
A
- Decreased lung volumes (group-B beta-hemolytic strep pneumonia)
- Increased lung volumes (non group-B strep pneumonia)
22
Q
Bilateral granular opacities, low lung volumes, and pleural effusions in a newborn…
A
Think group-B beta-hemolytic neonatal pneumonia
Note: If there were increased lung volumes, then you would think non group-B pneumonia.
23
Q
Is group-B or non group-B strep pneumonia more associated with pleural effusions?
A
Non group-B strep neonatal pneumonia is more highly associated with pleural effusions (75% of cases)
Note: Group-B strep neonatal pneumonia is also highly associated with pleural effusions (25%) which can help distinguish it from surfactant-deficiency disease.
24
Q
Patchy, asymmetric perihilar opacities with pleural effusions and hyperinflation…
A
Think non Group-B strep neonatal pneumonia
25
Persistent pulmonary hypertension of the newborn
In utero, the pulmonary blood pressures are high (allowing blood to bypass the lungs). This high pulmonary pressure usually normalizes after the infant takes their first breath, but can persist.
Note: This can be primary (idiopathic) or secondary (due to hypoxia in the setting of meconium aspiration, pneumonia, etc.).
26
Linear lucencies on chest radiograph in a 6 day old infant being ventilated for surfactant-deficiency disease...
Think pulmonary interstitial emphysema (air escaping the alveoli and entering the interstitial/lymphatics due to high PEEP)
Note: This pt is likely to develop a pneumothorax if not corrected.
27
How can you differentiate pulmonary interstitial emphysema from bronchopulmonary dysplasia?
Pulmonary interstitial emphysema occurs in the first week of life (usually while ventilated)
Bronchopulmonary dysplasia occurs in pts older than 2-3 weeks of life
Note: Both can present with linear lucencies on chest radiograph.
28
Treatment for pulmonary interstitial emphysema
- Switch ventilation methods (e.g. decrease PEEP)
- Place the infant with the affected side down (if PIE on the left, then place them left side down)
29
Linear lucencies on the chest radiograph of a 20 day old infant being ventilated for surfactant-deficiency disease
Think bronchopulmonary dysplasia (AKA chronic lung disease)
Note: If this infant were less than 1 week old, then you would think pulmonary interstitial emphysema.
30
Alternating regions of fibrosis (band-like opacities) and hyper aeration in an ex-premature infant who had prolonged ventilation...
Think bronchopulmonary dysplasia (AKA chronic lung disease)
31
Post-term infant with respiratory distress...
Think meconium aspiration
32
Term infant delivered by cesarean section with respiratory distress...
Think transient tachypnea of the newborn
33
Term infant born to a mother who received sedation during delivery with respiratory distress...
Think transient tachypnea of the newborn
34
Preterm infant with respiratory distress...
Think surfactant-deficiency disease (respiratory distress syndrome)
35
What are the major causes of pulmonary hypoplasia?
- Primary (idiopathic)
- Secondary (e.g. congenital diaphragmatic hernia, etc.)
36
What are the major causes of secondary pulmonary hypoplasia?
- Things taking up too much space within the chest (e.g. congenital diaphragmatic hernia, neuroblastoma, giant congenital heart, sequestration, etc.)
- Thinks outside the chest pushing on the chest (e.g. messed up rib cage such as in Jeune syndrome, large intraabdominal mass, etc.)
- Things outside the chest that mess up normal lung development (e.g. oligohydramnios such as in premature rupture of membranes, Potter sequence, renal problems, etc.)
37
Reduced fetal thoracic circumference during an OB ultrasound...
Think pulmonary hypoplasia (possibly secondary to oligohydramnios)
38
Fetal lung to head ratio < 1 on an OB ultrasound...
Think pulmonary hypoplasia (possibly secondary to congenital diaphragmatic hernia, skeletal issues, or oligohydramnios)
39
Potter sequence pathophysiology
Dysfunctional kidneys results in no urine output (no amniotic fluid), which prevents normal lungs from maturing (the fetus must breath the amniotic fluid for normal pulmonary development)
40
What is the most common congenital diaphragmatic hernia?
Bochdalek hernia ("B" in the Back of the diaphragm)
41
Bockdalek hernias are usually on the left, but Bochdalek hernias on the right are associated with...
Group-B strep pneumonia
42
Solitary, unilocular cyst abutting the trachea...
Think bronchogenic cyst
43
Bronchogenic cyst with an air-fluid level
Think infected bronchogenic cyst
Note: These usually do not communicate with the airway, so an air-fluid level should make you think infection.
44
Bronchopulmonary sequestration
Can be thought of as ectopic lung tissue that does not connect to the airways or pulmonary vasculature normally
Note: This can be intralobar or extralobar.
45
Bronchopulmonary sequestration tissue usually gets it blood supply from...
The aorta via a feeding artery
46
How can you differentiate intralobar from extralobar pulmonary sequestration on imaging?
You can't, the difference is extralobar sequestration is covered by a pleural lining and drains to systemic veins whereas intralobar has no pleural covering and drains to pulmonary veins (but you can't see either of these on imaging)
Note: The way to differentiate is by age and clinical presentation.
47
How can you differentiate intralobar from extralobar pulmonary sequestration?
Age and clinical presentation:
Recurrent infections in an adolescent (intralobar)
Respiratory distress/cyanosis in an infant (extrtalobar)
48
Which type of pulmonary sequestration is more often associated with other congenital anomalies?
Extralobar sequestration
Note: EXTRAlobar sequestration is associated with EXTRA things.
49
Extralobar sequestration is associated with...
- CCAMs
- Congenital diaphragmatic hernias
- Vertebral anomalies
- Congenital heart disease
- Pulmonary hypoplasia
Note: EXTRAlobar sequestration is associated with EXTRA things.
50
Where is intralobar pulmonary sequestration most often located?
- Left lower lobe (60%)
- Right lower lobe (40%)
51
Where is extralobar pulmonary sequestration most often located?
- Left lower lobe (90%)
- Subdiaphragmatic (10%)
52
Which pulmonary sequestration type usually presents with recurrent infections?
Intralobar
Note: The pleural covering of extralobar sequestration protects it from infections.
53
Where do pulmonary sequestrations drain veins to?
- Pulmonary veins (intralobar)
- Systemic veins (extralobar)
54
Recurrent pneumonia in the left lower lung...
Think intralobar pulmonary sequestration
55
Congenital lobar emphysema
When a bronchial pathology, such as bronchial atresia, leads to progressive air trapping resulting in a hyper lucent, hyper expanded lobe on radiographs that gets worse over time
56
What is the most common location for congenital lobar emphysema?
Left upper lobe
57
Treatment for congenital lobar emphysema?
Lobectomy
Note: The lobe with air trapping will not get better due to whatever bronchial pathology is causing the air trapping.
58
Question has a series of chest radiographs that show a left upper lobe opacity that resolves at the next time point and then has additional time points showing that where the opacity was is not getting hyper lucent and hyperexpanded, eventually causing mass effect on the mediastinum...
Think congenital lobar emphysema
59
CCAM
Congenital cystic adenomatoid malformation (AKA CPAM), a congenital malformation where lung tissue is replaced by dysfunctional adenomatoid tissue, usually only involving one lobe. The adenomatoid tissue does have a connection to the airway, which allows them to fill with air creating cystic spaces.
60
Time course of CPAM
AKA CCAM (congenital cystic adenomatoid malformation)
Most spontaneously decrease in size by the third trimester
61
Treatment for CCAM
Congenital cystic adenomatoid malformation (AKA CPAM)
Surgical removal of adenomatoid tissue (due to the small risk of malignant transformation to pleuropulmonary blastoma or rhabdomyosarcoma)
62
You see what looks like a CCAM and then identify a feeding artery from the aorta to the "adenomatoid" tissue...
Not CCAM, if there is an arterial feeder then it is a pulmonary sequestration
63
Cystic air spaces clustered in the left upper lobe of a kid...
Think congenital lobar emphysema (due to left upper lobe location)
Note: Could also be CCAM.
64
Cystic air spaces clustered in the left lower lobe of a kid...
Think pulmonary sequestration (due to left lower lobe location)
Note: Also look for a diaphragmatic hernia as these also favor the left lower lobe.
65
How can you differentiate a congenital pulmonary malformation from a primary lung tumor on MCQs?
Developmental/congenital pulmonary lesions in general are present on the second trimester screening ultrasound (if they tell you the 2nd trimester ultrasound was normal and now there is a pulmonary mass, think primary lung tumor
Note: This is a general rule, but there are exceptions.
66
What is the most common primary lung malignancy in children?
Pleuropulmonary blastoma
67
Child with a large right-sided, pleural-based pulmonary mass without chest wall invasion or calcifications (2nd trimester screening ultrasound was normal)...
Think pleuropulmomary blastoma (most common primary lung malignancy in children)
68
How can you distinguish a pleuropulmonary blastoma from an Askin/Ewing sarcoma in a child with a lung mass?
Both can appear as masses centered at the pleura, but Askin/Ewing sarcoma should have chest wall invasion (and PPB does not)
69
Pleuropulmonary blastomas are associated with...
Multilocular cystic nephrons (10%)
70
What is the most common primary lung mass in children?
Inflammatory myofibroblastic tumor (benign)
71
Child with a calcified, lobulated lung mass in the lower lobe...
Think inflammatory myofibroblastic tumor
72
Characteristic appearance of inflammatory myofibroblastic tumor on MRI
T2 bright (looks like fluid because they are composed of myxoid stroma)
73
What is the path of an umbilical venous catheter?
Umbilical vein -> left portal vein -> ductus venous -> hepatic vein -> IVC
74
What is the proper position for an umbilical venous catheter?
IVC-right atrium junction
75
Complications of umbilical venous catheter placement
- Hepatic infarction or portal hypertension (if malpositioned in a portal vein)
- Hepatic hematoma formation (if UVC erodes into the liver parenchyma)
76
What is the path of an umbilical artery catheter?
Umbilical artery -> iliac artery -> aorta
77
What is the proper position of an umbilical artery catheter?
T8-T10 (can also place lower at L3-L5)
Note: The important point is to not place the tip near the renal arteries, where it can cause thrombosis.
78
Complications of umbilical artery placement
Renal arterial thrombosis (which is why positioning is important)
79
How can you differentiate an umbilical venous catheter from an umbilical artery catheter?
The umbilical artery catheter courses inferiorly before turning around to go superior
80
Contraindication for an umbilical artery catheter
Omphalocele
81
What should you look for when evaluating umbilical artery catheter placement
- Catheter should remain left of midline on radiographs (in aorta)
- Tip should be at T8-T10 (or L3-L5)
82
Where should the catheters be for venoarterial ECMO?
- Right atrium (take deoxygenated blood)
- Aortic arch (give oxygenated blood)
Note: This can help rest the left ventricle, which doesn't have to pump as much blood in venoarterial ECMO.
83
Where should the catheters be for venovenous ECMO?
Both catheters in the right atrium (usually a dual lumen catheter)
Note: This only provides lung support, not the extra cardiac support that venoarterial ECMO can provide.
84
Chest radiographs demonstrate near complete white out of the bilateral lungs after initiating ECMO...
This is a normal finding (ECMO causes atelectasis and other physiological changes that looks like severe edema)
85
Complications of ECMO
- Hemorrhage (due to anticoagulation needed for ECMO)
- Brain bleeds (high risk due to anticoagulation and sick state of the pt)
86
What additional complication is possible for venoarterial ECMO that doesn't exist for venovenous ECMO?
Neurologic ischemic complications
Note: For venoarterial ECMO a carotid artery is usually sacrificed while placing the aorta catheter, leading to increased risk for neurogenic ischemic complications.
87
Classic imaging findings in viral pneumonia
- Peribronchial edema
- Air trapping
- Subsegmental atelectasis
88
What is the classic imaging finding seen in RSV infections?
Segmental or lobar atelectasis (particularly in the right upper lobe)
Note: In addition to the peribronchial edema seen in non-specific viral pneumonia.
89
5 y/o with a circular mass in the posterior lower lobes...
Think round pneumonia and recommend a follow up chest radiograph to confirm resolution
90
Round pneumonia is classically caused by...
Strep pneumoniae
Note: Only children (usually <8 y/o) get round pneumonia because you don't have good collateral ventilation pathways.
91
5 y/o with a rounded, pleural-based mass in the apex of the lung...
Think neonatal atypical peripheral atelectasis (similar to round pneumonia, but peripherally-based)
92
Centrilobular airspace opacities with fat attenuation in a child...
Think lipoid pneumonia and try to figure out what might have been aspirated
93
Expiratory radiographs demonstrate hyperlucency of the left lung that persists on left lateral decubitus views...
Air trapping in the left lung, suspicious for a bronchial foreign body in a child
94
Chest radiographs demonstrate hyperlucency of the left lung and the left lung appears smaller than the right lung (history of a prior viral lung infection)...
Think Swyer James (post-infectious obliterative bronchiolitis)
95
Multiple tracheal and lung nodules with some cavitation in a child...
Think papillomatosis
96
Papillomatosis is associated with a 2% risk of...
Squamous cell carcinoma
97
If you manipulate papillomatosis nodules...
You may cause dissemination of the HPV and cause more nodules
98
3 y/o with history of sickle cell disease and new opacities on chest radiograph...
Think acute chest due to sickle cell disease
99
What are imaging signs a kid might have sickle cell disease?
- Big heart
- Bone infarcts (look at the humeral heads)
- H-shaped vertebrae on lateral films
- Cholecystectomy clips
100
What is the pulmonary distribution of cystic fibrosis findings?
Apical predominance (lower lobes are less involved)
101
Classic chest imaging findings of cystic fibrosis
- Apical-predominant bronchiectasis
- Hyperinflation
- Pulmonary arterial hypertension
- Mucous plugging (lots of finger-in-gloving)
Note: Look for fatty replaced pancreas on CT and biliary cirrhosis.
102
Upper lobe predominant bronchiectasis in a child...
Think cystic fibrosis
103
Lower lobe predominant bronchiectasis in a child...
Think primary ciliary dyskinesia
104
Classic imaging findings of primary ciliary dyskinesia
- Lower lobe predominant bronchiectasis
- Situs inversus (50%; AKA Kartageners)
105
Why do cystic fibrosis and primary ciliary dyskinesia cause male infertility?
Males with cystic fibrosis are missing their Vas Deferens
Males with primary ciliary dyskinesia make sperm that can't swim
