Peds Flashcards
Craniosynostosis
“Craniosynostosis” is a fancy word for premature fusion o f one or several o f the cranial
sutures. The consequence o f this premature fusion is a weird looking head and face (with
resulting difficulty getting a date to the prom). Besides looking like a gremlin (or a coneheaded
extraterrestrial forced to live as a typical suburban human), these kids can also have
increased intracranial pressure, visual impairment, and deafness.
There are different named types depending on the suture involved - thus it’s worth spending
a moment reviewing the names and locations of the normal sutures.
Metopic suture
Bones Involved: frontal
Fusion direction: front to back
Fusion order: first ( 2-3months)
coronal suture
Bones Involved: frontal and parietal
Fusion direction: lateral to medial
Fusion order: second
lambdoid suture
Bones Involved: parietal and occipital
Fusion direction: lateral to medial
Fusion order: third
sagitaal suture
Bones Involved: parietal
Fusion direction: back to front
Fusion order: fourth
Sutures overview
• Sutures normally have a serrated (saw tooth) contour
• With early closure the suture will lose the serrated appearance - becoming more dense
and sharp. Eventually the suture will disappear completely.
• For the purpose of multiple choice, you should think about synostosis (early closure) as
likely syndromic - and focus your memorizing on this point.
• Having said that, sagittal and unilateral coronal synostosis are typically idiopathic
Metopic Synostosis
trigonocephaly
Eyes are close together (hypotelorism) Ethmoid sinuses underdeveloped Medial part of the orbit slants up Single suture synostosis most frequently associated with cognitive disorders (growth restriction of the frontal lobes)
“Quizzical Eye” appearance
sagittal syostosis
scaphocephaly or Dolichocephalic
Looks like an upside-down boat. Usually the kids have a normal IQ Usually the kids do NOT have hydrocephalus Associated with Marfans (both are tall and skinny).
most common form
coronal synostosis
brachycephaly
Unilateral subtype is more common.
Unilateral type causes the ipsilateral orbit to
elevate, and contralateral frontal bone to
protrude “frontal bossing”
Bilateral form is Rare - should make you think
syndromes (Borat s brother Bilo *).
“HarlequinEye” * if unilateral.
lambdoid synostosis
turricephaly
Tall Cranium (oxycephaly, acrocephaly) See Next Page for Unilateral Discussion
Least
Common
Form
Plagiocephaly
This word basically means “flat.” You will see it used to describe unilateral coronal synostosis as “anterior plagiocephaly You will see it used to describe unilateral lambdoid synostosis as “posterior plagiocephaly. ” The problem is that many people use the word “plagiocephaly” to describe the specific entity of “deformationalplagiocephaly ’’ - which is just benign positional molding, not a pathologic early closure. On the following page, I’ll go into more detail on this. Just know you may be required to read the question writer’s mind when the word is used to differentiate between the benign and pathologic entities.
POSITIONAL
PLAGIOCEPHALY
Infants that sleep on the same side every night develop a flat spot on the preferred dependent area of the head (occipital flattening). Onset: Weeks After Birth Ipsilateral Ear: Anterior Frontal Bossing: Ipsilateral Most common cause of an abnormal skull shape in infant Management is conservative (sleep on the other side for a bit)
LAMBDOID
CRANIOSYNOSTOSIS
I f this is bilateral think underlying Rhombencephalosynapsis Onset: Birth Ipsilateral Ear: Posterior / Inferior Frontal Bossing: Contralateral Rare as Fuck Management is Surgery
THIS vs THAT: Positional Plagiocephaly vs True Unilateral Lambdoid Synostosis
next step
Outside of the jungle (or the year 1987), the
diagnosis of synostosis is going to be made with
CT + 3D. If asked what test to order I would say
CT with 3D recons. Having said that, they could
show you a skull plain film (from 1987) and ask
you to make the diagnosis on that.
If the test writer was feeling particularly cruel
and bitter he/she could show the diagnosis
with ultrasound. In that case, remember that
a normal open suture will appear as an
uninterrupted hypoechoic fibrous gap
between hyperechoic cranial bones (Bright -
Dark - Bright, Bone - Suture - Bone).
Although certain MR gradient sequences can
be used, MRI has traditionally been
considered unreliable in identifying sutures
individually.
THIS vs THAT: Positional Plagiocephaly vs True Unilateral Lambdoid Synostosis
trivia
^or PurPose muP’ple choice, there are numerous random bone buzzwords that are supposed to elicit the reflexive diagnosis NF-l in your brain when you hear / read them. The more common ones include: • Absence / Dysplasia of the Greater Sphenoid Wing, • Tibial Pseudoarthrosis, • Scoliosis, and • Lateral Thoracic Meningocele. I’d like to add "bone defect in the region o f the lambdoid suture ” or the “asterion defect ” to that list of reflex generators. It’s rare and poorly described - therefore potentially high yield.
Clover Leaf Skull Syndrome
• Also referred to as Kleeblattschadei for the purpose of
fucking with you
• Contrary to what the name might imply - this complex
deformity is not associated with an increased ability to hit
green lights, reliably find good parking spots, or win the
lottery. I think that’s because the shape is more 3 leaf clover,
and not 4 leaf. One might assume, a head shaped like a 4 leaf clover
would probably be luckier.
• Instead, this deformity is characterized by enlargement o f the head
with a trilobed configuration, resembling a three-leaved clover.
• Results from premature synostosis o f coronal and lambdoid sutures
(most commonly), but often the sagittal closes as well.
• Hydrocephalus is a common finding.
• Syndromic Associations: Thanatophoric dysplasia, Apert syndrome
(severe), Crouzon syndrome (severe)
Clover Leaf Skull Syndrome
what sutures are closed
All the sutures are
closed
except the metric
and squamosal
Additional Craniosynostosis Syndromes
Most of the time (85%) premature closure is a primary (isolated) event, although
it can occur as the result o f a syndrome (15%). The two syndromes worth having
vague familiarity with are Apert’s and Crouzon’s
Apert’s
- Brachycephaly (usually)
• Fused Fingers (syndactyly) - “sock hand’
Crouzon’s
- Brachycephaly (usually)
- 1 st Arch structures (maxilla and mandible hypoplasia).
- Associated with patent ductus arteriosus and aortic coarctation.
- Short central long bones (humerus, femur) - “rhizomelia”
- Chiari 1 malformations 3: -70% of cases
Convolutional Markings
Normal gyral impressions on the inner table of the skull. You see them primarily during normal rapid brain growth (age 3-7). Usually mild and favors the posterior skull. If you see them along the more anterior skull then you should think about a “copper beaten” skull from the increased intracranial pressure.
Copper Beaten
The same thing as convolutional markings (the normal gyral impressions), just a shit ton more of them. You also see them along the anterior portions of the skull not just the posterior. Think about things that cause increased intracranial pressure. Classic examples: • Craniosynostosis • Obstructive Hydrocephalus
Luckenschadel - “L a c u n a r”
Oval, round, and finger shaped defects (craters) within the inner surface of the skull Different than Copper Beaten in that: (A) They aren’t gyrifonn. (B) They aren’t related to increased ICP. (C) They are usually present at birth. Instead they are the result of defective bone matrix. Classic Association: • Chiari II malformation / Neural Tube Defects.
lytic Skull Lesions
Lytic skull lesions in kids can come from a couple o f different things (LCH, Infection, Mets,
Epidermoid Cysts, Leptomeningeal Cysts, etc…). The two 1 want you to focus on are LCH and
the Leptomeningeal Cyst (which I will discuss later in the chapter).
LCH
(Langerhans Cell Histiocytosis) - Too many fucking dendritic cells - with local invasion. It
is a sorta pseudo malignancy thing. Nobody really understands it…. For the purpose of the exam
think about this as a beveled hole in the skull. The skull is the most common bone involved with
LCH. It is a pure lytic lesion (no sclerotic border). The beveled look is because it favors the
inner table. It can also produce a sequestrum o f intact bone (“button sequestrum).
lytic skull lesions
gamesmanship
If they tell you (or infer) the kid has neuroblastoma
- think about a met.
Parietal Foramina
These paired, mostly round, defects in the
parietal bones represent benign congenital
defects. The underlying cause is a delayed or
incomplete ossification in the underlying
parietal bones.
They can get big and confluent across the
midline. Supposedly, (at least for the big ones -
> 5mm) they are associations with cortical and
venous anomalies.
Wormian Bones
In technical terms, there are a bunch o f extra squiggles around the lambdoid sutures.
“Intrasutural Bones” they call them.
These things are usually idiopathic - however, if
you see more than 10 you should start thinking
syndromes.
Wormian Bones
gamesmanship
< 10 = Idiopathic
> 10 = First think Osteogenesis Imperfecta
> 10 + Absent Clavicle = Cleidocranial Dysostosis
Wormian Bones
Ddx
There is a massive differential, but 1 would just remember these “PORK-CHOP”
Pyknodysostosis Osteogenesis Imperfecta Rickets Kinky Hair Syndrome (Menke s / Fucked Copper Metabolism) Cleidocranial Dysostosis Hypothyroidism / Hypophosphatasia One too many 21 st chromosomes (Downs) Primary Acro-osteolysis (Hajdu-Cheney)
Dermoid / Epidermoid of the Skull
In the context of the skull, you can think about these things as occurring from the congenital misplacement of cells from the scalp into the bony calvarium. The result is a growing lump o f tissue (keratin debris, skin glands, etc...) creating a bone defect with benign appearing sclerotic borders. There are a few differences between the two subtypes that could be potentially testable (contrasted masterfully in the chart).
Although, I suspect a “what is it ? ” type question is more likely. As such, look through some google image examples to prepare yourself for that contingency.
Epidermoid
Histology:Only Skin
(Squamous
Epithelium)
Age of onset:Present between
age 20-40
Location: Present between
age 20-40
CT: CSF Density
MRI:T1 Variable,
T2 Bright,
NO Enhancement
Dermoid
Histology: Skin + Other Stuff
Like Hair Follicles,
Sweat Glands Etc
Age of onset:Typically have an
earlier presentation
Location: end to be midline.
The skin ones tend to
he around the orbits.
Associated with
Encephaloceles -
especially when
midline
CT: - More Heterogeneous,
- Calcifications
(internal or peripheral)
may be present
MRI: T2 Bright,
+/- Wall Enhancement
Congenital Dermal Sinus
Usually when people talk about these things they are referring to the spina bifida style
midline lumbosacral region defects. However, we are going to stay focused on the skull /
face. The two classic locations for dermal communications with the dura are the occiput and
the nose. Both of which are classically midline, and can be associated with a dermoid cyst.
For gamesmanship, consider a sinus tract anytime you see a cyst in these locations.
Dural communication will require
communication through the foramen cecum.
Sinus tracts may or may not have associated dennal or intraosseous cysts. Cysts may or may not have sinus tracts
THIS vs THAT: Scalp Trauma
There are 3 scalp hematoma subtypes. Because the subtypes are fairly similar, there is a high
likelihood a sadistic multiple choice writer will attempt to confuse you on the subtle
differences
Subgaleal Hemorrhage
Location:Deep to the Aponeurosis
(between aponeurosis and
periosteum)
Suture:NOT limited by
suture lines
Trivia: Covers a much larger area
than a cephalohematoma
Complications:Potentially life-threatening
- rapid blood loss.
Often not seen until 12-72
hours post delivery.
Cause: vacuum extraction
Cephalohematoma
Location: Under the Periosteum
(skin o f the bone)
Suture: Limited by suture lines
(won i cross sutures)
Trivia:Outer border may calcify as a rim
and leave a deformity - sorta like
a myositis ossificans
Complications:Usually requires no intervention (resolves within a few weeks) Can get super infected (E.Coli). Abscess would require drainage. Can cause skull osteomyelitis
Cause:Instrument or Vacuum Extraction
Caput Succedaneum
Location:Subcutaneous
Hemorrhage
(superficial to
the aponeurosis)
Suture:NOT limited by
suture lines
Trivia:Requires no
intervention
(resolves within
a few days)
Cause: prolonged delivery
Skull Fractures
Accidental (and non-accidental) head trauma is supposedly (allegedly, allegedly) the most common
cause of morbidity and mortality in children. As you might imagine, the pediatric skull can fracture
just like the adult skull - with linear and comminuted patterns. For the purpose of multiple choice, I
think we should focus on the fracture patterns that are more unique to the pediatric population:
Diastatic, Depressed, and “Ping-Pong”
Diastatic Fracture
This is a fracture along / involving the suture. When they intersect it is usually
fairly obvious. It can get tricky when the fracture is confined to the suture itself. The most common
victim of this sneaky fracture is usually the Lambdoid, followed by the Resident reading the case on
night float .. .with Attending backup (asleep in bed). How does one know there is traumatic injury to
a suture ? Classically, it will widen. This is most likely to be shown in the axial or coronal plane so
you can appreciate the asymmetry ( > 1 mm asymmetry relative to the other side).
Depressed Fracture
This is a fracture with inward displacement of the bone. How much inward
displacement do you need to call it “depressed” ? Most people will say “equal or greater to the
thickness of the skull.” Some people will use the word “compound” to describe a depressed
fracture that also has an associated scalp laceration. Those same people may (or may not) add the
word “penetrating” to describe a compound fracture with an associated dural tear.
Will any o f those people be writing the questions ? The dark side clouds everything. Impossible to
see the future is.
Ping Pong Fracture
outcomes
Ping Pong fractures typically have a favorable / benign clinical outcome
(depressed fractures have high morbidity).
Ping Pong Fracture
etiology
Diastatic and depressed fracture types usually require a significant wack on
the head. Where as “ping pong” fractures often occur in the setting of birth trauma
(Mom’s pelvic bones +/- forceps).
Ping Pong Fracture
imaging appearnce
Ping Pong fractures are hard as fuck to see. To show this on a
test you’d have to have CT 3D recons demonstrating a smooth inward deformity. You
could never see that shit on a plain film. I can’t imagine anyone being a big enough
asshole to ask you to do that. Hmmm…. probably.
Ping Pong Fracture
This is actually another subtype of depressed fracture but is unique in that it is
a greenstick or “buckle” type of fracture.
NEXT STEP
Depressed Fx
Unlike linear fractures (which usually heal without complication),
depressed fractures often require surgery. Some general indications Fracture
for surgery would include:
Depression of the fragments > 5mm (supposedly fragments more
than 5mm below the inner table are associated with dural tears),
Epidural bleed
Superinfection (abscess, osteomyelitis)
“Form” (cosmetic correction to avoid looking like a gargoyle),
“Function” (if the frontal sinus is involved, sometimes they need
to obliterate the thing to avoid mucocele formation).
Non-Accidental Trauma t Abusive Head Trauma)
Although car wrecks and falls account for the majority o f skull fractures in children, there still remains the timeless truth — some people just can’t take screaming kids. For the purpose of multiple choice, the follow clues should make your spider-sense tingle. • Inconsistent History: “My 7 month old wrecked his bike ” • Subdural Hematoma • Retinal hemorrhage • DAI / Parenchymal Contusion • Cerebral Edema, Stroke (less specific but still worrisome) • Depressed Skull Fx, or Fracture Crossing Suture Line (less specific but still worrisome)
Non-Accidental Trauma t Abusive Head Trauma)
gamesmansship
Subdurals have a stronger association with NAT
relative to epidurals. Think about vigorous
shaking (trying to get that last drop of ketchup
out of the bottle) tearing bridging cortical veins.
“Look High, Look Low”
- Sneaky Ways to Suggest NAT -
- Look High: Thrombosed (hyperdense)
cortical vein at the vertex
- Look Low: Retroclival hematoma (thin
hyperdense sliver in the pre-pontine region)
- Look Lower: Edema within the cervical soft
tissues
THIS VS THAT:
Retroclival Hematoma
Epidural
Below the Tectorial
Membrane
Subdural
Above the tectorial Membrane
THIS vs THAT:
Extra Axial Fluid
Chronic Subdural
(CSF Density)
Medial Displacement
of Bridging Vein
(sometimes smashed and
not well seen).
Usually Unilateral.
If Bilateral Usually
Asymmetric in Size.
Prominent CSF Spaces
Cortical veins are
adjacent to the inner table
Usually Symmetric
Enlarged extra-axial fluid spaces
Extra-axial fluid spaces are considered enlarged if they are
greater than 5 mm. BESSI is the name people throw around
for “benign enlargement of the subarachnoid space in infancy.’
The etiology is supposed to be immature villa (that’s why you
grow out of it).
THIS vs THAT:
BESSI vs Subdural Hygroma
BESSI - Cortical veins are adjacent to the inner table - they are usually seen secondary to enlargement o f the subarachnoid spaces (positive cortical vein sign) Subdural - Cortical veins are displaced away from the inner table - they are often not se
BESSI Trivia:
• It’s the most common cause of macrocephaly,
• Typically presents around month 2 or 3, and has a strong
male predominance.
• Typically resolves after 2 years with no
treatment,
• There is an increased risk of subdural bleed -
either spontaneous or with a minor trauma. This
subdural is usually isolated (all the same blood
age), which helps differentiate it from nonaccidental
trauma, where the bleeds are often of
different ages.
Enlarged extra-axial fluid spaces
trivia
Pre-mature kids getting tortured on ECMO often get enlarged extra-axial spaces. This isn’t really the same thing as BESSI but rather more related to fluid changes / stress.
Bessi imaging
Enlarged symmetric subarachnoid spaces favoring the anterior aspect o f the brain (spaces along the posterior aspect o f the brain are typically normal).
Brain parenchyma is normal and there is either normal ventricle size or very mild
communicating hydrocephalus. Communicating meaning that all 4 ventricles are big.
Periventricular leukomalacia I Hypoxic-Ischemic Encephalopathy of the Newborn
overview
This is the result of an ischemic / hemorrhagic injury, typically from a hypoxic insult during
birthing. The kids who are at the greatest risk are premature and little (less than 1500 g). The
testable stigmata is cerebral palsy - which supposedly develops in 50%. The pathology favors
the watershed areas (characteristically the white matter dorsal and lateral to the lateral
ventricles).
Periventricular leukomalacia I Hypoxic-Ischemic Encephalopathy of the Newborn
The milder finding can be very subtle. Here are some tricks:
The milder finding can be very subtle. Here are some tricks:
(1) Use PreTest Probability: The kid is described as premature or low birth weight.
(2) Brighter than the Choroid: The choroid plexus is an excellent internal control. The
normal white matter should always be less bright (less hyperechoic) when compared to the choroid
(3) “Blush” and “Flaring” : These are two potential distractors that need to be differentiated
from legit grade 1 PVL. “Blush ” describes the physiologic brightness of the
posterosuperior periventricular white matter - this should be less bright than choroid, and
have a more symmetric look. “Flaring” is similar to blush, but a more hedgy term. It’s the
word you use if you aren’t sure if it’s real PVL or just the normal brightness often seen in
premature infants white matter. The distinction is that “flaring” should go away in a
week. Grade 1 PVL persists > 7 days.
Periventricular leukomalacia I Hypoxic-Ischemic Encephalopathy of the Newborn
quick
Early: P e riv en tric u la r W h ite M a tte r N e c ro sis
(hyperechoic relative to choroid)
S u b acu te: C y s t F o rm a tio n
Periventricular leukomalacia I Hypoxic-Ischemic Encephalopathy of the Newborn
trivia
The most severe grade (4), which has subcortical cysts, is actually more common in
full term infants rather than preterms.
Periventricular leukomalacia I Hypoxic-Ischemic Encephalopathy of the Newborn
The later findings are more obvious with the development of cavitary periventricular cysts.
The degree of severity is described by the size and distribution of these cysts. These things take
a while to develop - some people say up to 4 weeks. So, if they show you a day 1 newborn
with cystic PVL they are leading you to conclude that the vascular insult occurred at least 2
weeks prior to birth (not during birth - which is often the case).
Germinal Matrix Hemorrhage ( GMH)
I like to think about the germinal matrix as an embryologic seed that sprouts out various
development cells during brain development. Just like a seed needs water to grow, the
germinal matrix is highly vascular. It’s also very friably and susceptible to stress.
Additionally, premature brains suck at cerebral blood flow auto-regulation. Mechanism:
Fragile vessels + too much pressure/flow = bleeds
An important thing to understand is that the germinal matrix is an embryological entity. So it
only exists in premature infants. As the fetus matures the thing regresses and disappears.
By 32 weeks, germinal matrix is only present at the caudothalamic groove.
By 36 weeks, you basically can’t have it (if no GM, then no GM hemorrhage).
Germinal Matrix Hemorrhage ( GMH)
Take home point
No GM Hemorrhage in a full term infant.
Germinal Matrix Hemorrhage ( GMH)
Gamesmanship
Similar looking bleed in a full term infant say “choroid plexus
hemorrhage” (not GMH).
Germinal Matrix Hemorrhage ( GMH)
scenario
The scenario will always call the kid a premature infant (probably earlier than 30 weeks). The
earlier they are bom the more common it is. Up to 40% occur in the first 5 hours, and most
have occurred by day 4 (90%). A good thing to remember is that 90% occur in the first week.
Germinal Matrix Hemorrhage ( GMH)
screening
Head US is used to screen for this pathology. Testable trivia includes:
• Who should be screened? Premature Infants (<32 weeks, < 1500 grams), Premature Infants
with Lethargy, Seizures, Decreased Hematocrit or a history o f “he don’t look so good.”
• When do you do the head US? First week o f life (remember this is when 90% o f them occur).
Some people will tell you - “first week and first month” (but that varies from institution).
Some people will also say - “every kid gets a head US prior to discharge from the NICU” - but
that is mainly done to detect PVL (not necessarily GMH).
Germinal Matrix Vs Choroid Plexus
Choroid Plexus is bright (hyperechoic) on ultrasound. Blood is also bright (hyperechoic).
You tell them apart based on their location. Choroid should not extend anterior to the junction o f the caudate and the thalamus (the so called caudothalamic groove).
This is the location o f the germinal matrix.
If you see bright stuff there - that is your grade 1 bleed.
This could also be shown with MR1 (T1 bright = bleed), same location.
Germinal Matrix Hemorrhage ( GMH)
Grading System (1-4) -
1 - Blood at the caudothalamic groove 2 - Blood in the ventricles but no dilation. 3 - Blood in the ventricles with dilation 4 - Blood in the brain parenchyma (from venous infarct)
Few additional things you should see at least once
prior to the exam. Do yourself a favor and
google images o f the following
- Caudothalamic groove in the coronal plane
- Grade 2,3,4 Bleeds
- Subependymal Cysts on US
- Porencephalic Cysts on US
- Choroid Plexus Cysts on US
- Ventricular coarctation on US - this is a mimic
Secondary Consequences GMH
Grade 1
Subependymal hemorrhage either results in a subependymal cyst or resolution or to a grade 2
Secondary Consequences GMH
Grade 2/3
Intraventricular hemorrhage results in hydrocephalus or grade 4
Secondary Consequences GMH
Grade 4
intraparenchymal hemorrhage either goes to a porencephalic cyst or hydrocephalus.
Choanal Atresia
Results from a membrane that separates the nasal cavity from its normal communication with the oral cavity. It is
usually unilateral but can be bilateral. The bilateral ones have a history
of “cyclical cyanosis that improves with crying ” (they mouth breath
when they cry). The unilateral classic stories are “can’t pass NG
tube, ” and “respiratory distress while feeding” (neonates have to
breath through their noses). You will also sometimes hear a history of
“a continuous stream o f snot draining from one or both nostrils, ” or
the word “rhinorrhea. ”
Choanal Atresia
types
There are two different types: bony (90%), and
membranous (10%). The appearance is a
unilateral or bilateral posterior nasal narrowing,
with thickening of the vomer.
Choanal Atresia
trivia
There are many syndromic associations
including CHARGE. Crouzons, DiGeorge,
Treacher Collins, and Fetal Alcohol Syndrome.
CHARGE is the one people mention the most.
CHARGE
Coloboma, Heart defect, Atresia (Choanal) Retarded growth, Genitourinary abnormalities Ear anomalies
Congenital Piriform Aperture Stenosis
This results from abnormal development of the medial nasal eminences,
and subsequent failure of formation of the primary palate. You can
see this in isolation or with choanal atresia. The piriform aperture of
the nasal cavity (bony inlet of the nose) is stenotic (as the name
suggests), and the palate is narrow. The classic picture is the
associated central maxillary “MEGA-incisor.” Midlinc defects
of the brain (corpus callosum agenesis, and holoprosencephaly) are
associated
— as my Grandma always said “face predicts brain ”.
Congenital Piriform Aperture Stenosis
next step
You have to image the brain
Congenital Piriform Aperture Stenosis
big thing to know
The big thing to know is the high association with hypothalamicpituitary-
adrenal axis dysfunction.
Ectopic Thyroid
Thyroid topics will be covered again in the endocrine chapter. 1 do want to mention one or two now for
completeness. To understand ectopic thyroid trivia you need to remember that the thyroid starts
(embryology wise) at the back of the tongue. It then descends downward to a location that would be
considered normal. The “pyramidal lobe” actually represents a persistence of the inferior portion of the
thyroglossal duct - that is why this thing is so variable in appearance. Sometimes this process gets all
fucked up and the thyroid either stays at the back of the tongue (lingual thyroid) or ends up half way
down the neck or even in the chest (ectopic thyroid).
Ectopic Thyroid
trivia to know
- Most “developed” countries test for low thyroid at birth (Guthrie Test). That will trigger a workup for either ectopic tissue or enzyme deficiencies.
- Nukes (1-123 or Tc-MIBI) is superior to ultrasound for diagnosing ectopic tissue. This is by far the most likely way to show this on a multiple choice exam. I guess CT would be #2 - remember thyroid tissue is dense because of the iodine.
- Ultrasound does have a preoperative role in any MIDLINE neck mass - with the point of ultrasound being to confirm that you have a normal thyroid in a normal place. If you resect a midline mass (which turns out to be the kids only thyroid tissue) you can expect an expensive well rehearsed didactic lecture on pediatric neck pathology from an “Expert Witness” sporting a $500 haircut.
- Lingual thyroid (back of the tongue) is the most common location of ectopic thyroid tissue
Thyroglossal Duct Cyst
As we discussed previously, thyroid related pathology can occur
anywhere between the foramen cecum (the base of the tongue)
and the thyroid gland. In this situation we are talking about the
duct (which is the embryological thyroid interstate highway to the
neck) failing to involute fully. What you get is a left over cyst -
hence the name. The classic locations are (1) at the base of the
tongue, and (2) midline anterior to the hyoid. Now textbooks will
make a big deal about these things becoming slightly lateral below
the hyoid. Do NOT get hung up on that. For the purpose of multiple
choice remember these guys are midline. Midline is the buzzword.
Thyroglossal Duct Cyst
things to know
- Classic Buzzword / Scenario = Midline Cyst in the Neck o f a Kid.
- Next step once you find one = confirm normal thyroid location and/or look for ectopic tissue (Ultrasound +/-Tc-M1BI, or 1-123).
- They are cystic (it’s not called a “Duct Solid”)
- Enhancing nodule within the cyst = CANCER (usually papillary)
- They can get infected.
Dermoid Cyst
It is true that dermoids almost always occur below the clavicles, but
when they do happen in the neck they have a pretty classic look:
midline sublingual / submandibular space with a “sac of marbles”
appearance. The marbles are lobules of fat within fluid.
Branchial Cleft Cyst (BCC)
Another cystic embryologic remnant. There are a bunch o f types (and subtypes… and subsubtypes)
and you can lose your fucking mind trying to remember all o f them - don’t do that.
Just remember that by far the most common is a 2nd Branchial Cleft Cyst (95%). The angle
of the mandible is a classic location. They can get infected, but are often asymptomatic.
Extension o f the cyst between the ICA and ECA (notch sign) just above the carotid
bifurcation is pathognomonic.
Branchial Cleft Cyst (BCC)
what is it
Most likely on CT or MR1. Ultrasound would be tough, unless they clearly
labeled the area “lateral neck” or oriented you in some other way.
Branchial Cleft Cyst (BCC)
location
They could (and this would be super mean) ask you the relationship o f a type 2 based on other neck anatomy. So - posterior and lateral to the submandibular gland or lateral to the carotid space, or anterior to the sternocleidomastoid. How I would handle that? Just remember it’s going to be lateral to everything. Lateral is the buzzword
Branchial Cleft Cyst (BCC)
mimic
They could try and trick you into calling a necrotic level 2 lymph node a BCC. Thyroid cancer (history o f radiation exposure) and nasopharyngeal cancer (history ofHPV) can occur in “early adulthood.” If you have a “new” BCC in an 18 year old - it’s probably a necrotic node. Next Step = Find the cancer +/- biopsy the mother fucker.
I say LATERAL
cyst in the neck,
you say
branchial cleft cyst
1 say MIDLINE
cyst in the neck,
you say
thyroglossal duct cyst
Jugular Vein Pathology
Septic Thrombophlebitis
clotted jugular vein. You see this classically in the setting of a
recent pharyngeal infection (or recent ENT surgery).
Jugular Vein Pathology
Septic Thrombophlebitis
what is it
Showing the clotted vein with the appropriate clinical history.
Jugular Vein Pathology
Septic Thrombophlebitis
“Lemierre’s Syndrome”
Seeing if you know that it has a fancy syndrome name.
Jugular Vein Pathology
Septic Thrombophlebitis
Next Step
Looking in the lungs for septic emboli. This could also be done in the reverse. Show
you the septic emboli, give you a history of ENT procedure (or recent infection), and have you ask
for the US of the neck veins.
Jugular Vein Pathology
Septic Thrombophlebitis
USMLE Step I Association Trivia
Fusobacterium necrophorum is the bacteria that causes the
septic emboli. As this bacteria sounds like a Marvel Comic villain the likelihood of it being asked
increases by at least 5x.
Jugular Vein Pathology
Phlebectasia
Idiopathic dilated jugular vein.
Jugular Vein Pathology
Phlebectasia
What is it
showing the dilated vein
Jugular Vein Pathology
Phlebectasia
trivia 1
is it not related to a stenosis. there aren o other signs of venous congestion
Jugular Vein Pathology
Phlebectasia
trivia 2
It gets worse with the Valsalva maneuver - “neck mass that enlarges with valsalva. ”
Both lymphatic and venous malformations can both look like a large transspatial
multicystic mass in the neck. They can both have fluid levels.
If you must try and tell them apart - you could try this:
• Venous Malformations will have enhancement of the cystic spaces.
• Lymphatic Malformations will have enhancement of the septa.
• Phlcboliths — suggests venous.
Hemangioma of Infancy
These things are actually the most common congenital lesions in the head and neck. Just like
any hemangioma they contain vascular spaces with varying sizes and shapes. Most people
consider them a “tumor” more than a vascular malformation.
Hemangioma of Infancy
how they look
Super T2 bright, with a bunch of
flow voids. Diffusely vascular on doppler.
Hemangioma of Infancy
phases
Typically they show up around 6 months of age, grow for a bit, then plateau, then involute (6-10 years). Usually they require no treatment.
Hemangioma of Infancy
indications for treatment
Large size / Rapid growth
with mass effect on the airway or adjacent vascular structures. Fucking with the kids eye movement or eyelid opening.
Hemangioma of Infancy
treatment
Typically medical = Beta blocker
propranolol
Hemangioma of Infancy
associations
PHACES Syndrome (discussed later in the chapter)
Cystic Hygroma (Lymphangioma)
This is another cystic lesion o f the neck, which is most likely to be shown as an OB
ultrasound (but can occur in the Peds setting as well). The classic look / location is a cystic
mass hanging off the back o f the neck on OB US (or in the posterior triangle if CT/MR1).
Cystic Hygroma (Lymphangioma)
associations
Turners (most common association).
Downs (second most common association).
Aortic Coarctation (most common CV abnormality), Fetal Hydrops (bad bad bad outcomes).
Cystic Hygroma (Lymphangioma)
septations
worse outcome
Cystic Hygroma (Lymphangioma) t2
T2 Bright (like a hemangioma). Does NOT enhance (hemangiomas typically do).
Fibromatosis Coli (“Congenital Torticollis”)
overview
This is a benign “mass” of the sternocleidomastoid
in neonates who present with torticollis (chin points
towards the opposite side - or you could say they
look away from the lesion). It’s really just a benign
inflammation that makes the muscle look crazy big.
Ultrasound can look scary, until you realize it’s just
the enlarged SCM. Ultrasound is still the best
imaging test. Sometimes it looks like there are two
of them, but that’s because the SCM has two heads.
It goes away on its own, sometimes they do passive
physical therapy or try and botox them.
Fibromatosis Coli (“Congenital Torticollis”)
trivia
• Most common cause of a neck “mass” in infancy
• Classic scenario is a 4 week old with a palpable neck mass and torticollis toward the affected side
• Best imaging test = US.
• Things that make you think it’s not FC: mass is outside the SCM, or internal calcifications - in
which case you should think to yourself… nice try Mother fuckers- that’s a neuroblastoma.
Fibromatosis Coli (“Congenital Torticollis”)
gamesmanship
So… there can be significant fuckery with the “direction” things curve or people look depending
on how the question is ask. What do I mean ?
If you made the mistake of just memorizing the word “towards” in association with fibromatosis
coli you might get tricked if the options were: A - Patient looks towards the involved side.
B - Patient looks toward the uninvolved side. You’d run into the same problem with the word
“away.”
Now, that might seem obvious once I spell it out like that but I’m pretty sure at least a few of you
were making a flashcard that had only the word “towards” on it. You have to assume the test
writer has the worst intentions for you. Don’t provide them with any opportunity to trick you.
Rhabdomyosarcoma
Although technically rare as fuck, this is the most common mass in the masticator space of a kid.
Having said that if you see it in the head/neck region is almost always in the orbit. In fact, its the most
common extra-occular orbital malignancy in children (dermoid is most common benign orbital mass
in child). The most classic scenario would be an 8 year old with painless proptosis and no signs of
infection.
What do sarcomas look like?
I’ll talk about this more in the MSK chapter, but in general I’ll just say they look mean as cat shit
(enhancing, solid, areas of necrosis, etc..).
Croup
This is the most common cause o f acute upper airway obstruction in young children. The
peak incidence is between 6 months and 3 years (average 1 year). They have a barky
“croupy” cough. It’s viral. The thing to realize is that the lateral and frontal neck x-ray is
done not to diagnosis croup, but to exclude something else. Having said that, the so-called
“steeple sign ” - with loss o f the normal lateral convexities o f the subglottic trachea is your
buzzword, and if it’s shown, that will be the finding. Questions are still more likely to center
around facts (age and etiology).
Croup
culprit
The culprit is often parainfluenza virus.
Epiglottitis
In contrast to the self-limited croup, this one can kill you. It’s mediated by H. Influenza and
the classic age is 3.5 years old (there is a recent increase in teenagers - so don’t be fooled by
that age). The lateral x-ray will show marked swelling o f the epiglottis (thumb sign). A fake
out is the “omega epiglottis” which is caused by oblique imaging. You can look for thickening
o f the aryepiglottic folds to distinguish.
Epiglottitis
trivia
Death by asphyxiation is from the aryepiglotic folds (not the epiglottis)
Exudative Tracheitis (Bacterial Tracheitis)
This is an uncommon but serious (possibly deadly) situation that is found in slightly older
kids. It’s caused by an exudative infection o f the trachea (sorta like diptheria). It’s usually
from Staph A. and affects kids between 6-10.
Exudative Tracheitis (Bacterial Tracheitis)
buzzword
linear soft tissue filling defect
within the airway.
Croup
quick
6 months - 3 years
(peak 1 year)
Steeple Sign: loss o f the normal
shoulders (lateral convexities) of
the subglottic trachea
Viral
(Most Common - parainfluenza)
epiglottitis quick
Classic = 3.5 years, but now
seen with teenagers too
Thumb Sign: marked
enlargement o f epiglottis
h. flu
Exudative tracheitis quick
6-10 years
Linear soft tissue filling
defect (a membrane) seen
within the airway
Staph A
Retropharyngeal Cellulitis and Abscess
I’ll just say quickly that you do see this
most commonly in young kids (age 6 months -12 months). If they don’t show it on CT, they
could show it with a lateral x-ray demonstrating massive retropharyngeal soft tissue
thickening. For the real world, you can get pseudothickcning when the neck is not truly lateral
To tell the difference between positioning and the real thing, a repeat with an extended neck is
the next step.
Subglottic Hemangioma
Hemangiomas are the most common soft tissue mass in the
trachea, and they are most commonly located in the subglott
region. In croup there is symmetric narrowing with loss of
shoulders on both sides (Steeple Sign). In contradistinction,
subglottic hemangiomas have loss of just one o f the sides.
Subglottic Hemangioma
Trivia
- Tends to favor the left side
- 50% are associated with cutaneous hemangiomas
- 7% have the PHACES syndrome
PHACES
P- Posterior fossa (Dandy Walker) H- Hemangiomas A- Arterial anomalies C- Coarctation o f aorta, cardiac defects E- Eye abnormalities S- Subglottic hemangiomas
Laryngeal Cleft
This is a zebra. The classic scenario is contrast appearing in the tracheal without laryngeal penetration
(aspiration). They could also show you a “thin tract of contrast extending to the larynx or trachea.” This
entity is a communicating defect in the posterior wall of the larynx and the esophagus or anterior hypo
pharynx. There arc a bunch of different cleft classifications - 1 can’t imagine that shit is appropriate for
the exam.
Laryngeal Cleft
trivia
• This is a thing - maybe google a Fluoro swallow picture of it
• These things have other complex malformations associated with them (usually GI)
• It is very tricky to call it with certainty on a swallow exam - definite diagnosis is always made with
direct visualization / scope (so a next step type question would recommend endoscopy to confirm).
airway papilloma
If you see a lobulated grape looking thing in the airway - think Papilloma, especially if the lungs are full of nodules (solid and cavitated). When 1 say Papilloma, You say HPV - typically from
perinatal (birth canal) transmission. These things are usually multiple (papillomatosis) and therefore have
multiple areas of airspace disease (atelectasis ect.). Some potential gamesmanship — because these thing
are typically multiple you will have more areas of air trapping then you would compared with an
aspirated crayon (or green bean), or even a solitary endobronchial lesion like a carcinoid. Multiple areas
of air trapping - think Papillomatosis over carcinoid or a foreign body. Having said that the nodules are a
more common finding… lots of them.
- G am e sm a n s h ip -
F ro n ta l an d L a te ra l N e c k R a d io g ra p h s
For the frontal, there are
two main things to think
about.
(1) Croup and
(2) Subglottic
Hemangioma
You can tell them apart
by the shouldering.
If you can’t tell…. try
and let the history bias
you. Cough? Fever?
Think Croup.
- G am e sm a n s h ip -
F ro n ta l an d L a te ra l N e c k R a d io g ra p h s
For the lateral, there are 4 main things to think about:
epiglottitis
retropharygeal abscess
tonsis (adenoids)
exudative tracheitis
lateral radiograph
epiglottitis
Looks like a
thumb
If the ordering suspects the diagnosis, do NOT bring this kid to x-ray. Have them do a portable.
lateral radiograph
retropharyngeal abscess
Too wide ( > 6mm at C2, or > 22mm at C6) Next Step = CT don't forget to look in the mediastinum for “Danger Zone” extension.
lateral radiograph
tonsils (adenoids)
Not seen till about
3-6 months, and not
big till around 1-2
years.
Too big when they
encroach the airway
lateral radiograph
exudative tracheitis
Linear Filling
Defect
It’s usually staph
Know how to tell if a neonatal chest is hyper-inflated or not. Don’t get hung up on this
low vs normal - that’s a bunch o f bologna. Just think (a) Hyper-inflated, or (b) NOT
Hyper-inflated.
The easiest way to do this is to just count ribs. More than 6 Anterior, or 8 Posterior as they intersect the diaphragm is too much. As a quick review, remember that the anterior ribs (grey) are the ones with a more sloping course as they move medially, where as the posterior ribs (black) have a horizontal course.
Other helpful signs suggesting
hyperinflation:
- Flattening o f the diaphragms
* Ribs take on a more horizontal appearance
Know what “Granular” looks like. Know what “Streaky” or “Ropy” looks like. My
good friends at Amazon are not capable of printing a clear picture o f these so I want you
to stop reading and
A. Go to google images
B. Search “Granular neonatal chest x-ray.’” Look at a bunch o f examples. Maybe even
download a few of them for review.
C. Search “Streaky Perihilar neonatal chest x-ray.” Look at a bunch o f examples.
Maybe even download a few o f them for review.
D. Search “Ropy neonatal chest x-ray.” Look at a bunch o f examples. Maybe even
download a few o f them for review.
Chest
random pearl
We are going to talk about the presence o f a pleural effusion as a
discriminator. One pearl is to look fo r an accentuated (thick) minor fissure on the right. If
you see that shit, kid probably has an effusion. Confirm by staring with fierce intensity at the
lung bases to look for obliteration o f the costophrenic sulcus.
High Volumes
+ Perihilar Streaky
Alphabet - MNoP
Meconium Aspiration
Non GB Neonatal
Pneumonia
Not High (low or
normal) Volumes
+ Granular
SSD
Group B Pneumonia
Meconium Aspiration
This typically occurs secondary to stress (hypoxia), and is more common in term or postmature
babies (the question stem could say “post term ” delivery). The pathophysiology is all
secondary to chemical aspiration.
Meconium Aspiration
trivia
- The buzzword “ropy appearance” o f asymmetric lung densities
- Hyperinflation with alternative areas o f atelectasis
- Pneumothorax in 20-40% o f cases
Meconium Aspiration
hyperinflation
How can it have hyperinflation?? Aren V the lungs fu l l o f sticky shit
(literally) ??? The poop in the lungs act like miniature bal 1-valves
(“floaters” 1 call them), causing air trapping - hence the increased lung
volumes.
Meconium Aspiration
reality vs multiple choice
“Meconium Staining ” on the amniotic fluid is common (like 15% o f all
births), but development o f “aspiration syndrome” is rare with only 5% o f those 15% actually have
aspiration symptoms. Having said that, if the question header bothers to include “Green colored
amniotic fluid” or “Meconium staining” in the question header they are giving you a major hint.
Don’t overthink a hint like this. I f they ask “What color was George Washington s white horse ? ” the
answer is NOT brown.
Transient Tachypnea of the Newborn (TTN)
The classic clinical scenario is a history o f c-section (vagina squeezes the fluid out of lungs
normally). Other classic scenario histories include “diabetic mother” and/or “maternal
sedation.” Findings are going to start at 6 hours, peak at one day, and be done by 3 days. You
are going to see coarse interstitial marking and fluid in the fissures.
Transient Tachypnea of the Newborn (TTN)
trivia
- Classic histories: C-Section, Maternal Sedation, Maternal Diabetes
- Onset: Peaks at day 1, Resolved by Day 3
- Lung Volumes - Normal to Increased
Surfactant-Deficient Disease (SDD)
This is also called hyaline membrane disease, or RDS. It’s a disease of pre-mature kids. The idea
is that they are bom without surfactant (the stuff that makes your lungs stretchy and keeps alveolar
surfaces open). It’s serious business and is the most common cause of death in premature
newborns. You get low lung volumes and bilateral granular opacities (just like B-hcmolytic
pneumonia). But, unlike B-hemolytic pneumonia you do NOT get pleural effusions. As a piece
of useful clinical knowledge, a normal plain film at 6 hours excludes SDD.
Surfactant Replacement Therapy
They can spray this crap in the kid’s lungs, and it makes a huge difference (decreased death rate
etc…). Lung volumes get better, and granular opacities will clear centrally after treatment. The
post treatment look of bleb-like lucencies can mimic PIE.
Surfactant Replacement Therapy
trivia
- Increased Risk of Pulmonary Hemorrhage
* Increased Risk of PDA
Neonatal Pneumonia (Beta-Hemolytic Strep - or “GBS”)
This is the most common type of pneumonia in newborns. It’s acquired during exit of the dirty
birth canal. Premature infants arc at greater risk relative to term infants. It has some different
looks when compared to other pneumonias (why I discuss it separately).
Neonatal Pneumonia (Beta-Hemolytic Strep - or “GBS”)
trivia
- It often has low lung volumes (other pneumonias have high)
- Granular Opacities is a buzzword (for this and SDD)
- Often (25%) has pleural effusion (SDD will not)
- LESS likely to have pleural effusion compared to the non Beta hemolytic version (25% vs 75%)
Neonatal Pneumonia (not Beta-Hemolytic Strep - “Non GB” or “Non GBS”)
Lots of causes. Typical look is patchy, asymmetric pcrihilar densities, effusions, and
hyperinflation. Will look similar to surfactant deficient disease but will be full term. Effusions are
also much more likely (they arc rare in SDD).
Persistent Pulmonary HTN
Also called “persistent fetal circulation”. Normally, the high pulmonary pressures seen in utero
(that cause blood to shunt around the lungs) decrease as soon as the baby takes his/her first breath.
Dr. Goljan (Step 1 wizard) calls this a “miracle,” and used this basic physiology to deny
evolution. When high pressures persist in the lungs it can be primary (the work of Satan), or
secondary from hypoxia (meconium aspiration, pneumonia, etc…). The CXR is going to show
the cause of the pulmonary HTN (pneumonia), rather than the HTN itself.
When I say “Post Term Baby, ”
You Say Meconium Aspiration
When I say “C-Section, ”
You say Transient Tachypnea
When I say “Maternal Sedation ”
You say Transient Tachypnea
When I say “Premature”
You say RDS
Solving Cases Using lung Volumes
High (flat diaphragms)
- Meconium Aspiration
- Transient Tachypnea
- Non BH Neonatal Pneumonia
Solving Cases Using lung Volumes
low
- Surfactant Deficiency (no pleural effusion)
* Beta-Hemolytic Pneumonia (gets pleural effusions)
Pulmonary Interstitial Emphysema (PIE)
When you have surfactant deficiency and they put you on a ventilator (which pulverizes your
lungs with PEEP), you can end up with air escaping the alveoli and ending up in the
interstitium and lymphatics. On CXR it looks like linear lucencies (buzzword). It’s a
warning sign for impending Pneumothorax. Most cases o f PIE occur in the first week of time
(bronchopulmonary dysplasia - which looks similar - occurs in patients older than 2-3
weeks). Surfactant therapy can also mimic PIE. The treatment is to switch ventilation
methods and/or place them PIE side down.
Pulmonary Interstitial Emphysema (PIE)
trivia
- Consequence of ventilation
- Usually occurs in the first week of life
- Buzzword = Linear Lucencies
- Warning Sign for Impending Pneumothorax
- Treatment is to put the affected side down
Pulmonary Interstitial Emphysema (PIE)
zebra
A total zebra is the progression of PIE to a large cystic mass. The thing can even cause
mediastinal mass effect.
Chronic Lung Disease - CLD / (Bronchopulmonary Dysplasia - BPD)
This is the kid bom premature (with resulting surfactant deficiency), who ends up being
tortured in ventilator purgatory. His/her tiny little lungs take a ferocious ass whipping from
positive pressure ventilation and oxygen toxicity — “barotrauma” they call it. This beating
essentially turns the lungs into scar, inhibiting their ability to grow correctly. That is why
people call this “a disease of lung growth impairment.”
Chronic Lung Disease - CLD / (Bronchopulmonary Dysplasia - BPD)
classic vignetter
Prolonged ventilation in a tiny (<1000 grams), premature kid (<32 weeks)
Chronic Lung Disease - CLD / (Bronchopulmonary Dysplasia - BPD)
classic look
Alternating regions of fibrosis (coarse reticular opacities), and hyper-aeration (cystic lucencies).
Chronic Lung Disease - CLD / (Bronchopulmonary Dysplasia - BPD)
buzzword
“Band like opacities”
Classic This vs That: CLD vs PIE
PIE = First week of life,
CLD = After 3 to 4
weeks’ postnatal age
Pulmonary Hypoplasia
This can be primary or secondary. Secondary causes seem to lend themselves more readily to multiple
choice questions. Secondary causes can be from decreased hemi-thoracic volume, decreased vascular
supply, or decreased fluid. The most common is the decreased thoracic volume, typically from a space
occupying mass such as a congenital diaphragmatic hernia (with bowel in the chest), but sometimes
from a neuroblastoma or sequestration. Decreased fluid, refers to the Potter Sequence (no kidneys ->
no pee -> no fluid -> hypoplastic lungs).
Bronchopulmonary Sequestration
These are grouped into intralobar and extralobar with the distinction being which has a pleural
covering. The venous drainage is different (intra to pulmonary veins, extra to systemic veins). You
can NOT tell the difference radiographically. The practical difference is age of presentation;
intralobar presents in adolescence or adulthood with recurrent pneumonias, extralobar presents in
infancy with respiratory compromise.
Bronchopulmonary Sequestration
intralobar overview
Much more common (75%). Presents
in adolescence or adulthood as recurrent pneumonias
(bacteria migrates in from pores of Kohn). Most
commonly in the left lower lobe posterior segment
(2/3s). Uncommon in the upper lobes. In
contradistinction from extralobar sequestration, it is
rarely associated with other developmental
abnormalities. Pathology books love to say “NO
pleural cover ” - but you can’t see that shit on CT or MR.
Bronchopulmonary Sequestration
intralobar quick
more common
presents in adolescence
recurrent infections
no pleural cover
pulmonary venous drainage
Bronchopulmonary Sequestration
extralobar overview
Less common of the two (25%).
Presents in infancy with respiratory compromise
(primarily because of the associated anomalies -
Congenital cystic adenomatoid malformation
(CCAM), congenital diaphragmatic hernia, vertebral
anomalies, congenital heart disease, pulmonary
hypoplasia). It rarely gets infected since it has its own
pleural covering. These are sometimes described as
part of a bronchopulmonary foregut malformation, and
may actually have (rarely) a patent channel to the
stomach, or distal esophagus. Pathology books love to
say “has a pleural cover ” - but you can’t see that shit
on CT or MR.
Bronchopulmonary Sequestration
extralobar quick
less common
presents in infancy
associated congenital anomalies
Bronchopulmonary Sequestration
gamesmanship
I say recurrent pneumonia in same area, you say intralobar sequestration.
Bronchogenic Cysts
Typically an incidental finding. They are generally solitary and unilocular. They typically do NOT communicate with the airway, so if they have gas in them you should worry about infection.
Congenital Cystic Adenomatoid Malformation (CCAM)
As the name suggests it’s a malformation of adenomatoid stuff that replaces normal lung. Most
of the time it only affects one lobe. There is no lobar preference (unlike CLE which favors the
left upper lobe). There are cystic and solid types (type 1 cystic, type 3 solid, type 2 in the
middle). There is a crop of knuckle heads who want to call these things CPAMs and have 5
types, which I ’m sure is evidence based and will really make an impact in the way these things
are treated. CCAMs communicate with the airway, and therefore at least components of them
can fill with air. Most of these things (like 90%) will spontaneously decrease in size in the third
trimester. The treatment (at least in the USA) is to cut these things out, because of the iddy bitty
theoretical risk of malignant transformation (pleuropulmonary blastoma, rhabdomyosarcoma).
What i f you see a systemic arterial feeder (one coming o ff the aorta) going to the CCAM ?
Then it’s not a CCAM, it’s a Sequestration. — mumble to yourself “nice try assholes”
Congenital Lobar Emphysema (CLE)
The idea behind this one is that you have bronchial pathology (maybe atresia depending on what
you read), that leads to a ball-valve anomaly and progressive air trapping. On CXR, it looks
like a lucent, hyper-expanded lobe.
Congenital Lobar Emphysema (CLE)
trivia
- It’s not actually emphysema - just air trapping secondary to bronchial anomaly
- It prefers the left upper lobe (40%)
- Treatment is lobectomy
Congenital Lobar Emphysema (CLE)
gamesmanship
•The classic way this is shown in case conference or case books is with a series of CXRs.
The first one has an opacity in the lung (the affected lung clears fluid slower than normal
lung). The next x-ray will show the opacity resolved. The following x-ray will show it
getting more and more lucent. Until it’s actually pushing the heart over.
Congenital Diaphragmatic Hernia (CDHs)
Most commonly they are Bochdalek type. B is in the Back - they are typically posterior and to
the left. The appearance on CXR is usually pretty obvious.
Congenital Diaphragmatic Hernia (CDHs)
trivia
- Usually in the Back , and on the left (Bochdalek)
- If it’s on the right - there is an association with GBS Pneumonia
- Mortality Rate is related to the degree o f pulmonary Hypoplasia
- Most have Congenital Heart Disease
- Essentially all are malrotated
Congenital Diaphragmatic Hernia (CDHs)
gamesmanship
•One trick is to show the NG tube curving into the chest.
Locational Strategy
Left Upper lobe
Think Congenital Lobar Emphysema (CLE) first But, remember CCAM has no lobar prevalence, so it can be anywhere
Locational Strategy
left lower lobe
Think Sequestration First
Congenital Diaphragmatic
Hernia (CDHs) favors this
side too
Special Situations in Peds Chests
viral
In all ages this is way more common than bacterial infection. Peribronchial edema is the
buzzword for the CXR finding. “Dirty” or “Busy” Hilum. You also end up with debris and mucus in
the airway which causes two things (1) hyperinflation and (2) subsegmental atelectasis. Respiratory
Syncytial Virus (RSV) - This will cause the typical non-specific viral pattern as well. However,
there is the classic testable predilection to cause a segmental or lobar atelectasis — particularly in the
right upper lobe.
Special Situations in Peds Chests
Round Pneumonia
Kids get round pneumonia. They love to show
this, and try to trick you into thinking it’s a mass. Younger than 8 you are
thinking round pneumonia, round pneumonia, round pneumonia - with S.
Pneumonia being the culprit. The PhD trivia is that these occur because you
don’t have good collateral ventilation pathways. Round pneumonia is
usually solitary, and likes the posterior lower lobes. Take home message: No
CT to exclude cancer, just get a follow up x-ray.
Special Situations in Peds Chests
Neonatal atypical peripheral atelectasis (NAPA)
It is best to think about this as a cousin or uncle of Round Pneumonia (they are in the
same family). It is essentially the same thing except it is peripheral. The
classic look is a round, pleural based “mass” in the apex of the lung.
Similarly to the “round pneumonia” this is a transient finding and will
resolve as the primary process improves.
Special Situations in Peds Chests
Lipoid Pneumonia
Classic history is a parent giving their newborn a teaspoonful of olive oil
daily to cultivate “a spirit o f bravado and manliness. ” Although this seems like a pretty solid plan, and
I can’t fault their intentions - it’s more likely to result in chronic fat aspiration. Hot Sauce is probably a
better option. Most people will tell you that bronchoalveolar lavage is considered the diagnostic
method of choice. CXR nonspecific - it is just airspace opacities. CT is much more likely to be the
modality used on the exam. The classic finding is low attenuation (-30 to -100 HU) within the
consolidated areas reflecting fat content
Special Situations in Peds Chests
Bronchial Foreign Body
The key concept is that it causes air trapping.
The lung may look more lucent (from air
trapping) on the affected side. You put the
affected side down and it will remain lucent
(from air trapping). Another random piece of
trivia is that under fluoro the mediastinum will
shift AWAY from the affected side on
expiration.
Special Situations in Peds Chests
Swyer James
This is the classic unilateral lucent lung. It typically occurs after a viral lung
infection in childhood resulting in post infectious obliterative bronchiolitis. The size of the affected
lobe is smaller than a normal lobe (it’s not hyper-expanded).
Special Situations in Peds Chests
Papillomatosis
Perinatal HPV can cause these soft tissue masses within the airway and lungs.
It’s also seen in adults who smoke. “Multiple lung nodules which demonstrate cavitation” is the
classic scenario. Some testable trivia includes the 2% risk of squamous cell cancer, and that
manipulation can lead to dissemination. The appearance of cysts and nodules can look like LCH
(discussed more in the thoracic chapter), although the trachea is also involved.
Special Situations in Peds Chests
Sickle Cell I Acute Chest
Kids with sickle cell can get “Acute chest.” Acute chest actually
occurs more in kids than adults (usually between age 2-4). This is the leading cause of death in sickle
cell patients. Some people think the pathology is as such: you infarct a rib -> that hurts a lot, so you
don’t breath deep -> atelectasis and infection. Others think you get pulmonary microvascular
occlusion and infarction. Regardless, if you see opacities in the CXR of a kid with sickle cell, you
should think of this.
Special Situations in Peds Chests
Cystic Fibrosis
So the sodium pump doesn’t work and
they end up with thick secretions and poor pulmonary clearance. The real damage is done by recurrent infections.
Special Situations in Peds Chests
Primary Ciliary Dyskinesia
The motile part of
the cilia doesn’t work. They can’t clear their lungs and get
recurrent infections. These guys have lots of bronchiectasis
just like CF. BUT, this time it’s lower lobe predominant
(CF was upper lobe
Bronchial foreign body
key point
A normal inspiratory CXR is meaningless. Don’t forget that the crayon / green bean is going
to be radiolucent. You need expiratory films to elicit air trapping. Normally, the bottom lung is gonna
turn white (move less air). If there is air trapping the bottom lung will stay black.
Sickle Cell I Acute Chest
gamesmanship
(how do you know it’s sickle cell?)
•Kid with Big Heart
•Kid with bone infarcts (look at the humeral heads)
•Kid with H shaped vertebra (look on lateral)
Cystic Fibrosis
things to know
•Bronchiectasis (begins cylindrical and progresses to
varicoid)
•It has an apical predominance (lower lobes are less
affected)
•Hyperinflation
•They get Pulmonary Arterial Hypertension
•Mucus plugging (finger in glove sign)
•Men are infertile (vas deferens is missing)
Cystic Fibrosis
trickery
• Fatty Replaced Pancreas on CT
• Abdominal Films with
Constipation
Biliary Cirrhosis (from blockage of intrahepatic bile ducts), and resulting portal HTN
Primary Ciliary Dyskinesia
Things to know
•Bronchiectasis (lower lobes)
•50% will have Kartageners (situs inversus). So, 50%
will not
•Men are infertile (sperm tails don’t work)
•Women are sub-fertile (cilia needed to push eggs
around)
This vs that
cystic fibrosis vs primary ciliary dyskinesia
CF: Upper Lobe Predominant - Brochiectasis Infertile - Men are Missing the Vas Deferens
Primary Ciliary dyskinesia: Lower Lobe Predominant - Bronchiectasis Infertile - Men’s Sperm Don’t Swim For Shit
Pleuropulmonary Blastoma (PPB)
This is a primary intrathroacic malignancy. They can look a lot like CCAMs and even have different types (cystic, mixed, solid). These
things are usually right sided, pleural based, and without chest wall invasion or calcifications.
No rib invasion (helps distinguish it from the Askin / Ewing Sarcoma o f the Chest Wall - if
they won’t tell you the age), No calcification. The more solid types can have mets to the brain
and bones. The cystic type seem to occur more in kids less than a year old, and be more benign.
Pleuropulmonary Blastoma (PPB)
things to know
- Big Fucking Mass (B.F.M.) in the chest o f a 1-2 year old
- Shouldn’t have an eaten-up rib (Askin tumors often do)
- 10% o f the time they have a multilocular cystic nephroma.
Umbilical Venous Catheter (UVC)
A UVC passes from the umbilical vein to the left
portal vein to the ductus venosus to a hepatic vein to
the 1VC. You don’t want the thing to lodge in the
portal vein because you can infarct the liver. The
ideal spot is at the 1VC - Right Atrium junction.
Development of a “Cystic Liver Mass” (Hematoma) can suggest
UVC erosion into the liver.
Umbilical Artery Catheter (UAC)
A UAC passes from the umbilicus, down to the
umbilical artery, into an iliac artery then to the aorta.
Positioning counts, as the major risk factor is renal
arterial thrombosis. You want to avoid the renal
arteries by going high (T8-T10), or low (L3-L5)
Things to know about UACs
- It goes down first
- It should be placed either high (T8-T10) or low (L3-L5)
- Omphalocele is a contraindication
UAC =
down then up
UVC =
straight up
ECMO - Extracorporeal Membrane Oxygenation
Neonatologists primarily use this device to torture sick babies - hopefully into revealing the
various government secrets they have stolen, or the location of their organization’s
underground lair. “Enhanced interrogation” or “temporizing measure o f last resort,” they call
it - to get around the Geneva Conventions.
Oh you want to pretend you can’t talk? Get the ECMO catheters!
Alternatively, it can be used as a last resort in neonatal sepsis, severe SSD, and meconium
aspiration. Actually, in cases of meconium aspiration ECMO actually does work (sometimes).
ECMO - Extracorporeal Membrane Oxygenation
types overview
There are two main types: (1) Veno-Arterial “V-A”,
and (2) Veno-Venous “V-V”
In both cases deoxygenated blood is removed from the
right atrium and pumped into a box (artificial lung) to
get infused with oxygen. The difference is in how it is
returned.
ECMO - Extracorporeal Membrane Oxygenation
V-A
In V-A, blood goes back to the Aorta (you can see why
this would help rest the left ventricle). The catheter is
usually placed at the origin o f the innominate or
“overlying the arch.”
ECMO - Extracorporeal Membrane Oxygenation
V-V
In V-V blood goes right back into the right atrium. In
this situation even if the lungs were totally clogged
with shit (meconium aspiration) and no oxygen
exchange was happening it wouldn’t matter because
the blood that is being pumped (RA -> RV ->
Pulmonary Artery) already has oxygen in it.
ECMO - Extracorporeal Membrane Oxygenation
V-A quick
Catheter Position: RA + Aorta (near the origin of the innominate artery)
Catheter Position: RA + Aorta (near the origin of the innominate artery)
ECMO - Extracorporeal Membrane Oxygenation
V-V quick
Catheter
Position:
RA+ RA
“Dual Lumen”
Lung Support
ECHO - Extracorporeal Membrane Oxygenation - Continued
Lung White Out = Normal
Mechanism is variable depending on who you asked. The way
1 understand it is that the airway pressure suddenly drops off causing atelectasis, plus you
have a change in the circulation pattern that now mimics the fetal physiology (mom =
artificial lung). Resulting oxygen tension changes lead to an edema like pattern. A multiple
choice trick could be to try and make you say it is worsening airspace disease, or reflects the
severity of the lung injury. Don’t fall for that. It’s an expected finding.
ECHO - Extracorporeal Membrane Oxygenation - Continued
Consequences of V-A
I mentioned on the prior page that they typically ligate the carotid
when they place the Arterial catheter. No surprise that they will be at increased risk for
neurologic ischemic complications as a result.
ECHO - Extracorporeal Membrane Oxygenation - Continued
Crucial Complication = Hemorrhage
The combination of anticoagulation (necessary in
ECMO) and being sick as stink puts these kids at super high risk for head bleeds. This is
why they will get screened for germinal matrix hemorrhage prior to being placed on ECMO
and then routinely screened with head ultrasounds (expertly read by the second year resident
on call).
Catheter Position Gamesmanship:
I think there are two likely ways a multiple choice question could be structured related to
ECMO catheter position. The first would be to show you a series of daily radiographs with the
latest one demonstrating migration of one or both catheters. Thats the easy way to do it.
The sneaky way would be to show you the
catheter with the lucent distal end and the dot
marker on the tip. This would be particularly
evil as there are tons of different catheter
brands and looks, but if I was going to try and
trick you, this would be the way that I would do
it.
In this case, the venous catheter looks falsely
high if judged by the lucent tip, but that round
metallic marker (near the black arrow) shows
the tip in the RA.
The arterial catheter “overlies the region of the
aortic arch,” which is normal.
mediastinal masses
anterior
Normal Thymus
Thymic Rebound
Lymphoma:
Germ Cell Tumor (GCT):
Normal Thymus
This is the most common mediastinal
“mass.” It’s terribly embarrassing to call a normal thymus a
mass, but it can actually be tricky sometimes. It can be
pretty big in kids less than 5 (especially in infants).
Triangular shape of the thymus is sometimes called the “sail
sign.” Not to be confused with the other 20 sail signs in
various parts of the body, or the spinnaker sail sign, which is
when pneumomediastinum lifts up the thymus.
Thymic Rebound
In times of acute stress (pneumonia, radiation, chemotherapy, bums), the
thymus will shrink. In the recovery phase it will rebound back to normal, and sometimes larger
than before. During this rebound it can be PET avid
Lymphoma:
This is the most common abnormal mediastinal mass in children (older
children and teenagers). Lymphoma vs Thymus can be tricky. Thymus is more in kids under 10,
Lymphoma is seen more in kids over 10. When you get around age 10, you need to look for
cervical lymph nodes to make you think lymphoma. If you see calcification, and the lesion has
NOT been treated you may be dealing with a teratoma. Calcification is uncommon in an untreated lymphoma.
Lymphoma:
complications
Compression o f SVC, Compression o f Pulmonary> Veins, Pericardial Effusion, Airway Compression.
Lymphoma:
all/leukemia
can appear very similar to Lymphoma (soft tissue mass in the anterior
mediastinum). In this scenario, most people will tell you that Lymphoma can NOT be
differentiated from Leukemia on imaging alone.
Germ Cell Tumor (GCT):
On imaging, this is a large anterior mediastinal mass arising from or at least next to the thymus. It comes in three main flavors,
Germ Cell Tumor (GCT):
teratoma
Mostly Cystic, with fat and calcium
Germ Cell Tumor (GCT):
seminoma
Bulky and Lobulated. “Straddles the midline ”
Germ Cell Tumor (GCT):
NSGCT
Big and Ugly - Hemorrhage
and Necrosis. Can get crazy and invade the lung.
Things that make you think the
thymus is a cancer!
• Abnormal Size for patients Age (really big in a 15 year old) • Heterogenous appearance • Calcification • Compression of airway or vascular structure
Middle mediastinal masses
lymphadenopathy
duplications cysts
lymphadenopathy
Middle mediastinal lymphadenopathy is most often from granulomatous disease (TB or Fungal), or from lymphoma.
Mediastinal Adenopathy Trivia
mononucleosis
Cause: EBV (-90%), CMV (-10%)
Classic Scenario: Adolescent with hilar adenopathy, splenomegaly,
and fatigue.
Trivia: Rash after Antibiotics (Amoxicillin)
Trivia: “No sports for 3 weeks” - to avoid splenic injury
Mediastinal Adenopathy Trivia
primary TB
Distribution of nodes in usually unilateral, right hilar, right paratracheal
Lower and Middle lobe consolidation is common
Mediastinal Adenopathy Trivia
histoplasmosis
Midwest and Southeast United States
Most have normal CXRs
Can have hilar adenopathy
Mediastinal Adenopathy Trivia
coccidioidomycosis
Southwest United States
Usually looks like consolidation and nodules
Can have hilar adenopathy
Mediastinal Adenopathy Trivia
lymphoma
Often cited as the “most common” anterior mediastinal mass in a kid. Hilar involvement (usually bilateral) is more common with Hodgkin
Mediastinal Adenopathy Trivia
sarcoid
Uncommon in children — it usually presents in the early-mid 20s.
Case reports of early onset Sarcoid exist.
Duplications cysts
These fall into three categories (a) bronchogenic, (b) enteric,
(c) neuroenteric. The neuroenterics are traditionally posterior mediastinal.
Duplications cysts
bronchogenic
water attenuation - close to the trachea or bronchus. Trivia:
• Tend to be middle mediastinal (70%), the rest are in the hilum
• Typically filled with mucus or fluid
Duplications cysts
enteric/esophageal
water attenuation close to the esophagus (lower in the
mediastinum). Trivia:
• Abutment o f the esophagus is the key finding.
• Can communicate with the lumen of the esophagus - and have air/fluid levels.
• Usually on the right, involving the distal esophagus
• Can be middle or posterior mediastinal in location
• Second most common G1 lumen duplication cyst (distal ileum #1)
Posterior mediastinal masses
Neuroblastoma
Ewing Sarcoma
Askin Tumor (Primitive Neuroectodermal tumor of the chest wall):
Neuroenteric Cyst
Extramedullary Hematopoiesis
Neuroblastoma
This is the most common posterior mediastinal mass in a child under 2. This
is discussed in complete detail in the GU PEDs section. I’ll just mention that compared to abdominal
neuroblastoma, thoracic neuroblastoma has a better outcome. It may involve the ribs and vertebral
bodies. Also, remember that Wilms usually mets (more than neuroblastoma) to the lungs, so if it’s in
the lungs don’t forget about Wilms.
Neuroblastic mediasetinal tumors
most aggressive and immature to least aggressive and mature
neuroblastoma > ganglioneruoblastoma > ganglioneuroma
When Compared with Neuroblastoma, Ganglioneuromas are
• Less Aggressive
• More Circumscribed (less invasive)
• Less Likely to have Calcifications (although they still can)
• Pound in Older Children
These tumors can NOT be differentiated with imaging alone
(but that doesn’t mean someone can’t write a multiple choice
question asking you to try).
Askin Tumor (Primitive Neuroectodermal tumor of the chest wall):
This is now considered part of the Ewing Sarcoma spectrum, and is sometimes called an Ewing
sarcoma of the chest wall. They tend to displace adjacent structures rather than invade early on (when
they get big they can invade). They look heterogenous, and the solid parts will enhance.
Neuroenteric Cyst
By convention these are associated with vertebral anomalies (think
scoliosis, hemivertebrae, butterfly vertebrae, split cord, etc..) - think cyst protruding out of an unsealed
canal / defect. The cyst does NOT communicate with CSF, is well demarcated, and is water density.
Favor the lower cervical and thoracic regions.
Extramedullary Hematopoiesis
This occurs in patients with myeloproliferative
disorders or bone marrow infdtration (including sickle cell). Usually, this manifests as a big liver and
big spleen. However, in a minority of cases you can get soft tissue density around the spine
(paraspinal masses), which are bilateral, smooth, and sharply delineated.
Extramedullary Hematopoiesis
This occurs in patients with myeloproliferative
disorders or bone marrow infdtration (including sickle cell). Usually, this manifests as a big liver and
big spleen. However, in a minority of cases you can get soft tissue density around the spine
(paraspinal masses), which are bilateral, smooth, and sharply delineated.
Strategy - The Anterior Mediastinal Mass
Lymphoma
In a kid just assume it’s Hodgkins (which means it’s gonna involve the
thymus). Why assume Hodgkins ? Hodgkins is 4x more common than NHL. Hodgkins
involves the thymus 90% of the time.
Strategy - The Anterior Mediastinal Mass
How the hell do you tell a big ass normal thymus in a little baby vs a lymphoma?
My main move is to go age. Under 10 = Thymus, Over 10 = Lymphoma.
Strategy - The Anterior Mediastinal Mass
Thymic Rebound
If the test writer is headed in this direction they MUST either (a)
bias you with a history saying stuff like “got off chemo” or “got off corticosteroids” or
(b) show you a series of axial CTs with the thing growing and maintaining normal
morphology. I think “a” is much more likely.
Strategy - The Anterior Mediastinal Mass
The Funk
In general just think morphology / density:
• Soft Tissue - Kinda Homogenous = Think Lymphoma or Hyperplasia
• Fat = Germ Cell Tumor (Why God!? Why Klinefelters!?)
• Water = Congenital Stuff - Think Lymphangiomas
Strategy - The Posterior
Mediastinal Mass
Under 10
Think malignant,
Think neuroblastoma.
Strategy - The Posterior
Mediastinal Mass
Think benign.
If it’s a round mass- Think about
Ganglioneuromas & Neurofibromas
If it’s cystic (and there is scoliosis) think
Neuroenteric Cyst
If they show you coarse bone
trabeculation - with an adjacent mass (or
a history of anemia) - Think
Extramedullary Hematopoiesis
Strategy - The B.F.M.
“Big Fucking Mass” If you see a B.F.M. in the chest o f a kid, you basically have two choices: (1) Askin Tumor (PNET / Ewings) - * AGE 10+, look for an eaten up rib. (2) Pleuropulmonary Blastoma *AGE is typically less than 2.
Esophageal Atresia /TE fistula:
This can occur in multiple subtypes, with the classic ways of showing it being a frontal CXR with an NG tube stopped in the upper neck, or a fluoro study (shown lateral) with a blind ending sac or communication with the tracheal tree. There are 5 main subtypes, only 3 (shown above) are worth knowing (being familiar with) for the purpose of the exam.
Esophageal Atresia /TE fistula:
Things to know
•Diagnosis is made with a Fluoro swallow exam
•Most Important Thing To Know are the VACTERL associations (more on this later)
• The most common subtype is the N-Type (blind ended esophagus, with distal esophagus hooked up
to trachea
• Excessive Air in the Stomach = H type (can also be with N type)
• No Air in the Stomach = Esophageal Atresia
• The presence of a right arch (4%) must be described prior to surgery (changes the approach).
Esophageal Atresia /TE fistula:
gamesmanship
Fake out for TE fistula is simple aspiration. Look for the presence or absence of laryngeal penetration to tell them apart (if shown a dynamic Fluoro swallow exam).
VACTERL:
This is extremely high yield. VACTERL is a way of remembering that certain
associations are seen more commonly when together (when you see one, look for the others).
VACTERL:
frequency
V - Vertebral Anomalies (37%) A - Anal (imperforate anus) (63%) C - Cardiac (77%) TE - Tracheoesophageal Fistula or Esophageal Atresia (40%) R - Renal (72%) L - Limb (radial ray) - 58%
VACTERL:
diagnosis
VACTERL association is diagnosed when 3
or more of the defined anomalies affect a
patient.
Therefore, keep investigating when 1 -2 of
these anomalies are found.
The heart and kidneys are the most
commonly affected organs in this
VACTERL:
trivia
If both limbs are involved, then both kidneys tend to be involved. If one limb is involved, then
one kidney tends to be involved
Esophageal Atresia
stricture
Around 30% of kids with a repaired esophageal atresia will end up with a focal
anastomotic stricture. Strictures can also be seen with caustic ingestion (dishwashi
Esophageal Foreign Bodies
Kids love to stick things in their mouths (noses and ears).
This can cause a lot of problems including direct compression o f the airway, perforation, or even
fistula to the trachea. Stuff stuck in the esophagus needs to be removed.
Esophageal Foreign Bodies
The esophagus is a dirty sock, it flexes to accommodate that big piece of steak you didn’t even bother to chew. The trachea is rigid, like that math teacher I had in high school (who hated music… and colors), but unlike the math teacher it has a flexible membrane in the back.
The point of me mentioning this is to help you problem solve a “where is the coin ”
type question. The esophagus will accommodate the coin so it can be turned in any direction. The trachea is rigid and will force the coin to rotate
into the posterior membrane — so it will
be skinny in the AP direction.
Ingested Metallic Foreign Bodies
Magnets
One magnet is ok. Two or more magnets is a
problem. The reason is that they can attract
each other across intestinal walls leading to
obstruction, necrosis, perforation, and a law suit.
Surgical Consult
NOT an MRI (dumbass)
Ingested Metallic Foreign Bodies
AA or AAA Batteries
Less of a problem relative to other types of
batteries, but can cause serious problems if you
need them for the DVR control because Game of
Thrones season 7 is on (spoiler it sucked).
Serial plain film exams.
Remove if they stay in
the stomach for more
than 2 days
Ingested Metallic Foreign Bodies
Disc Batteries
They look like coins, except they have two rings. The literature is not clear, but it appears that modern batteries rarely leak (leaking is bad - caustic chemicals, heavy metals etc..).
Stuck in the esophagus
= big problem, gotta
get them out within 2 hours.
Stuck in the stomach =
problem, gotta get
them out within 4 days.
Ingested Metallic Foreign Bodies
Coins
(Including Pennies
minted prior to 1982)
Copper Pennies are relatively safe.
Make sure it is not a disc battery
(coins have one order ring, disc
battery has two).
Remove if: Retention in the esophagus for more than 24 hours or Stomach for more than 28 days.
Ingested Metallic Foreign Bodies
Pennies
-minted after 1982
Those minted after 1982 contain mostly Zinc
which when combined with stomach acid can
cause gastric ulcerations, and if absorbed in
great enough quantity can cause zinc toxicosis
(which is mainly pancreatic dysfunction /
pancreatitis). The ulcers are the more likely thing
to happen, so just remember that.
So how the hell can you tell the date of a penny
that is swallowed? Either (a) the question stem
will have to say something like - “2 year old child
playing with father’s collection of 1984 pennies” ,
or the more likely (b) showing you the penny with
characteristic radiolucent holes - from erosion.
remove rom stomach
