Hx: MVA

Would you like more images?

Is there just a single finding, or are there multiple findings?

Answer:

Transient Intussusception

An intussusception is when a segment of bowel is pulled either into itself or into an adjacent bowel loop due to peristalsis.
 
Classic teaching is there there is a "lead point", such as a mass, that gets "caught" by the normal bowel peristalsis. The peristalsis then pulls the mass and proximal bowel wall (aka intussusceptum) down through the more distal bowel (intussuscipiens) much like how food normally transits through the bowel.
 

Although the most common location of intussusceptions is ileocolic (ie distal ileum telescoping into the colon), they can occur anywhere (although gastric involvement is extremely rare).

• Entero-enteric (small bowel into small bowel)
• Entero-colonic (small bowel into colon - see above)
• Colo-colonic (colon into colon)
   

As one can imagine, this can lead to severe complications:

• bowel obstruction
• as the mesentery gets pulled in it can cause venous/arterial compromise -> bowel wall edema, ischemia and even necrosis
   

Although "Lead points" are often found in adults, they are infrequently found in children. Possibile lead points include but are not limited to:
 

• Tumor
  • benign (such as polyp, lipoma, GIST, mucocele)
  • malginant (such as colon cancer, lymphoma, metastatic disease)
• Developmental
  • Meckel's diverticulum
  • duplication cyst
• Hypertrophic Peyer's patches (GI lymphoid tissue)
  • Thought to be the the most common cause in children (not usually visualized macroscopically)
     

Clinical findings of pathologic intussusception

Classic findings include:

• intermittent abdominal pain
• vomiting
• Right upper quadrant "sausage-shaped" mass
• occult or gross rectal bleeding
  • classic description is "currant jelly stool" *this is concerning for undeerlying bowel ischemia/necrosis
     

Radiology

X-ray

• elongated soft tissue mass with proximal dilated bowel loops (ie bowel obstruction)

Flouroscopy

• similar findings as X-ray, but after giving oral contrast, the classic finding is the "coiled spring" appearance where you see oral contrast both within the lumens of the intussusceptum and intussuscipiens.

• The benefit of flouroscopy is real time imaging and the ability to perform interventions. In children this allows for real time reduction of the intussusception using air (or water soluble contrast) administered rectally. By creating a retrograde backpressure, one can "push" the intussuscepting loop backwards out of the intussuscipiens.

• Of course this should NOT be attempted if there is any concern of ischemia/necrosis (bloody/ currany jelly stool) or perforation (peritoneal signs, free air, etc)

Ultrasound

Ultrasound can be highly sensitive and specific and is ideal for children given it's lack of radiation. Look for:

• Target sign (aka bullseye sign) = rings of hyper- and hypo- echoic circles correlating to the alternating cross-sectional layers of mucosa (hyper-), submucosa (hypo-), and muscularis (hyper-) of the intussusceptum (inner layers) out through the intussuscepiens (outer layers)
• Peudokidney sign = longitudinal appearance of the intussuscepted loop within the lumen of the intusscepiens

CT

The modality of choice in adults.
 
When imaged in transverse cross-section, the appearance mimics the target (aka bullseye) sign above, showing the wall of the intusscepted loop, surrounded by the wall of the intussuscpiens.
 
When imaged longitudinally, one can actually see the bowel loop telescoping into the intussuscipiens in longitudinal cross-section.

Back to our case.

Did you find the intussusception? Did you perhaps find more than one?
 
I think I stopped counting at SIX instussecptions in this completely asymptomatic patient being scanned after an MVA (they had other significant extremity injuries). Are there even more?
 

Transient Instussusception

While all of the above is true, that all applies to pathologic intussusceptions. Here we have NO bowel dilation/obstruction, NO descrete lead points and NO bowel wall edema/hypoenhancement to suggest vascular compromise. Thus these are termed incidental or transient
intussusceptions.
 
My experience is that these are not uncommon. I can't even count the number of times (nonetheless the number of instussusceptions!) that I have encountered incidentally on asymptomatic patients, often after motor vehicle accidents (correlation? causation? who knows). But again, as long as there was no concerning findings listed above, they have all resolved, even on extremely short term follow up (even within the time between aterial and portal venous imaging!)
 
While I do tend to mention these in my report, I try to be explicit that they are extremely likely to be transient/incidental in the abscence of symptoms. And if/when the doc calls with concern, you can reassure them that unless the patient has symptoms listed above, they are verly likely to be resolved by the time you are talking.
 

If you'd like to see other examples, feel free to check out some older Wetread case below. The write-ups were much shorter then, but now they you know all about intussusceptions, it's the imaging that is important right?

Season 2 Case 40

History: Abdominal Pain

WetreadWetreadRad

Season 6 Case 6

Case 6History: abdominal pain h1 {text-align: center;} details > summary { padding: 4px; width: 100%; background-color: #eeeeee; border: none; box-shadow: 1px 1px 2px #bbbbbb; cursor: pointer; } details > p { background-color: #eeeeee; padding: 4px; margin: -5px; cursor:pointer;…

WetreadWetreadRad

History: Dementia, poor food intake

Answer:

Bilateral Mandibular Dislocation

If you came of Radiology age before the ubiquitous use of CT, you may have seen these; however these days, mandible series are quite rare (and perhaps deservedly so). My experience is that these days few Rads feel very comfortable with them.

Anatomy

Here is a normal lateral view of the mandible/skull.
 
Green = temporomandibular fossa (aka glenoid fossa)
* anterior border is the articular tubercle (aka condylar eminence)
* posterior border is the tympanic portion of the temporal bone (behind which is the external auditory canal
 
Blue = mandibular condyle
 
Here you can see the mandibular condyle sitting in the glenoid fossa. There is a normal articular disc that sits between the cartilage of the mandibular condyle and the cartilage of the glenoid fossa which of course we just see as space on X-ray.

So if there is injury, or the capsule is loose from prior injury or degeneration, it is possible for the mandibular condyle to dislocate of the glenoid fossa, almost always anteriorly.

Posterior and superior (into the intercranial fossa) dislocations are rare.

Our Patient

So lets look again at our patient.

Again, I've labeled the mandibular condyles and the temporomandibular fossa (aka glenoid fossa) for both sides.

Hopefully you can now see that BOTH the right and the left condyles are dislocated ANTERIOR to the fossa. For once symmetry is NOT your friend :(

But just in case you don't believe me:

And for completeness, here is the axial CT labeled and centered on the left TMJ.

Our patient here had a history of prior dislocations so the CT was ordered for initial diagnosis and then the X-rays were ordered to confirm reduction. Unfortunately it was not reduced (which they suspected clinically).
 
They re-attempted reduction, which they believed to be successful, without additional imaging.

Movement

Movement of the TMJ is complex and can cause some confusion with dislocations. While MRI evaluation of the disc and motion is beyond the scope of this write-up, it is important to remember that the condyle normally moves forward with opening but it should not move beyond the lowest point of the articular tubercle. That is dislocation!

Why CT?

For all new dislocations (or concerns for dislocation), I would recommend utilizing CT for diagnosis, not just because of the limited experience with X-rays, but because you should always be on the lookout for a fracture (such as transcondylar, of the coronoid process, or even the glenoid fossa if there is significant trauma). These can be difficult to impossible (glenoid fx) to see on X-rays and of course management changes significantly.
 
*Plus, in the instance of trauma, you get to check out all the other bones of the face just in case.

Management

If you are interested in the management, here is a nice ER doc review:

Temporomandibular Joint (TMJ) Dislocation

This post discusses TMJ dislocations and the numerous reduction techniques.

Core EMSee My Posts

Hx: Hand Pain

It sure would be nice to know an actual location for the patient's pain, wouldn't it?

Would you like more images?

Answer:

Gamekeeper's Thumb

Gamekeeper's thumb (ie skier's thumb) is a tear or avulsion of the ulnar collateral ligament (UCL) of the first metacarpophalangeal joint.
 
Radiopedia distinguishes between the two of these such as:

• Skier's thumb is acute injury from traumatic hyperabduction (such as from a skier's pole planted in the ground)
• Gamekeeper's thumb is chronic, non-traumatic overuse injury (such as from wringing the necks of rabbits every day -Yes, this is the real origin)
   

Clinically, the injury is the extremely similar (and thus I conceptualize them almost the same). Either is due to acute vs repetitive hyperabduction at the first metacarpophalangeal joint leading to a tear of the UCL or avulsion of the UCL (typically from it's insertion on the medial aspect of the base of the first phalanx).

Okay, so it's a ligmentous/avulsion injury. Splint it an move on right?
 

Well the problem is the anatomy. The UCL lies deep to the adductor pollicis aponeurosis (ie the muscle that approximates your thumb to your hand). When the UCL is torn (or avulsed) the proximal (metacarpal) piece of the UCL can displace superficial to, the adductor pollicis aponeurosis preventing approximation, healing and union.
 

This is termed a Stener lesion and when this happens, surgery is now required to reapproximate the ligament for healing.
 

Classically MRI was the modality of choice for evaluating for Stener lesions, but more recently, Ultrasound is becoming increasingly popular for it's wider availability, cost, etc.
 

I do not have a lot of experience with Ultrasound so I'll leave that to experts below.

Do you have any great examples? please feel free to share!
 
@RyanChristieMD

Stener lesion | Radiology Reference Article | Radiopaedia.org

Stener lesions are seen in the context of a torn ulnar collateral ligament of the thumb’s metacarpophalangeal joint (gamekeeper’s thumb). Pathology Normally, the ulnar collateral ligament lies deep to the adductor pollicis tendon. A Stener les...

Radiopaedia.orgYahya Baba

VIDEO: Dynamic Ultrasound Evaluation for Soft-Tissue Injuries of the Extremities: Hand, Wrist, and Ankle : American Journal of Roentgenology: Vol. 214, No. 4 (AJR)

[email protected]

MRI of the Fingers: An Update : American Journal of Roentgenology: Vol. 213, No. 3 (AJR)

Madhavi Patnana

History: Flank pain

Would you like more images?

Answer:

Pyonephrosis

Pyo- (pus), -nephrosis (process of the kidney)

Pyonephrosis is exactly that . It is infection of the kidney where there is purulent material (pus) in the collecting system.

Complications:

• Renal Obstruction
• Renal abscess
• Xanthogranulomatous pyelonephritis
• Sepsis

Radiology

Ultrasound:

• hydronephrosis
• echogenic debris within the collecing system
• fluid-fluid levels within the collecting system
• dirty shadowing (from gas) within the collecting system

CT:

• Signs of infection + hydronephrosis
  • increased density in the collecting system
  • layering material (or excreted contrast) in the collecting system
  • gas in the collecting system
• Don't forget to look for typical signs of infection
  • perinephric stranding
  • heterogeneous renal enhancment (aka lobar nephronia)
  • Urothelial thickening/enhancement

MRI:

• similar findings as CT

Treatment:

Percutaneous nephrostomy + antibiotic therapy is the treatment of choice to drain the pus from the collecting system and relieve the obstruction.

Our Case

On both the axial and sagital images above, you can see the dilated collecting system with urine-pus level. Note the size of the right kidney is much larger than the left (from the obstruction/infection) with right perinephric stranding.
 

Perhaps you also noted the thick walled urinar bladder. Could that be simple redundant thickening of the bladder wall that is non-distended? Or could it be inflammatory thickening from cystitis? Fortunately if it is infection it will be treated by the antibiotics used to treat the upper urinary tract infection.

History: Abdominal Pain

Would you like more images?

Answer:

Large Bowel Lymphoma

Facts:

• Primary lymphoma of the colon is rare, comprising only ~1% of all colonic malignancies.
• On the contrary, the GI tract is the most common site of primary extra-nodal lymphoma (however still only ~1.5% of lymphomas).
• Of GI tract lymphomas, gastric lymphoma is the most common followed by small bowel, with large bowel lymphoma only comprising ~15% of GI tract lymphomas
• Most common type of colonic lymphoma is related to Non-Hodkin's lymphoma (NHL)
• Majority of primary colonic lymphomas arise in the right colon/cecum
• Majority of colonic lymphomas are single in location

Pathology:

• Most common etiology is Non-Hodgkin's lymphoma
  • diffuse large B-cell lymphoma subtype to be more specific
• Also associated with:
  • mucosa-associated lympoid tissue (MALT) lymphoma
  • mantle cell lymphoma
     
• Increased risk factors:
  • HIV/AIDS
  • Inflammatory bowel disease (IBD)
  • immunosuppression post transplant

Presentation:

• Colonic lymphoma most commonly presents in 40-60yo, with slight male predominance
• Main symptoms are:
  • weight loss
  • abdominal pain
  • rectal bleeding
  • abdominal mass
• Despite large size, perforation and obstruction tend to be rare

Findings:

• Can present as:
  • large intraluminal polypoid mass (most common)- can grow to extended through the wall into the peritoneal cavity
  • focal infiltrative tumor
  • aneurysmal dilatation
     

While perhaps not the most common, the classic Aunt-minnie appearance is that of marked, smooth, long segment circumferential wall thickening WITHOUT bowel obstruction
 

Overall, when compared to adenocarcinoma:

1. lymphoma tends to present with larger, longer segment lesions
2. the more common site is proximal colon, particularly around the ileocecal valve, compared to adenocarcinoma which tends towards the distal colon

Treatment:

• Of course it varies based upon location and subtype, but generally includes surgical debulking and systemic chemotherapy.
• Prognosis is still considered to be more directly related to surgical therapy than chemotherapy

Our Patient:

We can see a large amount of smooth, circumferential wall thickening of the distal transverse colon. Yet despite this, we still see stool passing through (ie it is non-obstructive).
 
This is an example of the classic "Aunt Minnie" finding I was taught, ie circumferential wall thickening with a patent lumen or even luminal dilation. Although it seems somewhat counter-intuitive saying colon mass with a dilated lumen, but the concept is that as the lymphoma infiltrates the interstinal wall, it destroys the myenteric plexus preventing muscular contraction, while also stretching the muscle fibers and destroying the microvasculature yielding to areas of necrosis (which then can lead to cavitation and "aneurysmal" appearance).

Radiological Features of Gastrointestinal Lymphoma

Gastrointestinal lymphomas represent 5–20% of extranodal lymphomas and mainly occur in the stomach and small intestine. Clinical findings are not specific, thus often determining a delay in the diagnosis. Imaging features at conventional and cross-sectional ...

PubMed Central (PMC)Giuseppe Lo Re

History: Abdominal Pain

Anything wrong with this picture?

Answer:

Answer: Backscatter Artifact

 
There are numerous types of imaging artifact in plain film radiography. Radiopaedia has a nice compilation here:

X-ray artifacts | Radiology Reference Article | Radiopaedia.org

X-ray artifacts can present in a variety of ways including abnormal shadows noted on a radiograph or degraded image quality, and have been produced by artificial means from hardware failure, operator error and software (post-processing) artifacts...

Radiopaedia.orgHenry Knipe

In our case, we see metallic radiodensities overlying the abdomen that are definitely suggestive of an electronic device. But where is it? Did the patient swallow something? It is rather large to swallow isn't it?
 

What we are seeing is the actual electronic components of the image detector. But why are we seeing it on this exam and not all exams?
 

Brief Background

 
This is by no means complete and probably contains some questionable oversimplifaction, but I think it provides a good starting point for those starting out.... or even just not super interested < wink>< wink>
 

Radiographs are created by sending a "beam" of X-rays through a patient (or patient's body part) in order to "see" what is on the inside.
 
X-rays are similar to visible light except there are just on a different spot of the electromagnetic spectrum. 

As you may know (or can see from above), the type of electromagnetic radiation changes based upon it's wavelength. And the wavelength of the radiation is inversely related to it's frequency. So as wavelength goes up, the frequency obviously goes down (there was this smart guy name Max Plank who figured this out in the early 20th century as part of we now call Quantum Mechanics).

 
For example: 

• Broadband radio is measured in kilometers (10^3) 
• Microwave radatiation is measured in micrometers (10^-6) 
• Visible light is measured in 100s of nanometers (10^-9) 
• X-rays are measured in single digit nanometers (10^-9) 
   
  So INVERSELY, X-rays have a HIGHER frequency, and thus a higher energy.

We can create these X-rays (often called "photons") using something similar to a light bulb. Using an electric current, we can create a stream of electrons flowing from the cathode (negative side) to the anode (positive side) of a circuit. If we stick a tungsten plate between them, the electrons will hit the tungsten and cause emission of X-rays!

So now that we have X-rays, what do we do with them?  Well shoot them at someone of course!

While visible light is relatively low energy and doesn't penetrate objects well, the higher energy X-rays can penetrate everyday material, and the degree of penetration/transmission depends upon the density of the specific material. The amount that is blocked increases (ie attenuated) as the density of the material increases (ie  Metal blocks the most > bone > muscle > fat > air which blocks very little). The photons that are able to fully penetrate through the material then hit an imaging cassette that is positioned on the opposite side from the X-ray source.

Raiography Basics

The process of Radiographic imaging has evolved a great deal through the decades.
 

Plain-Film Radiography

Originally we had a source (X-ray generator) and a cassette that contained actual film (film-screen radiography). A short burst of X-rays are sent through the patient. The X-rays that are able to fully penetrate through the object are able to hit the film, creating silver atoms in the film emulsion which turn the film black. The amount of "blackness" is determined by the quantity of X-rays that are able to get through that one particular spot, and thus dependent on the density at that one spot.
 
The more dense the material, the more attenuated the X-ray beam and thus the less X-rays get through, the less silver atoms get created and the less dark the image. Air = dark and Bone = light
 
More detail can be found here. Example of the cassette can be seen in image A below.
 

Computer Radiography

Technological advancements lead to Computed Radiography(CR). CR replaces the film component with an image plate composed of photostimulable phosphor. When exposed to the X-ray beam, electrons are excited into a higher energy state in proportion to the amount of exposure (ie the degree of transmission and thus the material's density). We can then release these excited electrons back to normal using a technique called photostimulation where specific wavelength lasers de-excite the electrons and release their energy which can be quantified and digitized it to "digital" radiographs.
 
These are the the cassettes that need to be exposed and then returned to a "reader" to obtain the digital image (image B below). So while nicer than plain film (and providing better contrast and detail), we are still stuck with 1 image per cassette before we head back to the department, read and reset everything. Wanna know more?

Digital Radiography

The most recent advancement is Digital Radiography (DR). DR was able to get rid of the readers by converting the image plate to a complete flat panel detector. These dectectors can work in a couple different ways but in all forms are able to convert X-rays directly to an electric charge (ie digital signal output) (more detail here). This electric signal can be directly measured, and similar to the CR, it will be proportional to the degree of transmission and thus the density of the material.
 
While DR provides for even higher contrast and other imaging benefits, one of the biggest benefits is now the exposure system is entirely self-contained. Build in a wifi connection and now your "images" can be instantly sent to the PACS even if you are roaming around doing AM portable X-rays. Once sent, you can erase the "image" and reuse the same cassette over and over.(image D below)  

Back to our case!

So what is backscatter artifact?

 
Well when the patient is larger and/or we need to cover a large area, it is necessary to increase the amount of X-rays used. Much like light that can reflect off shiny things, X-rays also refract or scatter when they hit things, going in varying directions beside just the one we want. So when these scattered X-rays actually go beyond the patient and scatter (reflect) back towards the patient, the cassette actually gets exposed from the wrong direction, with these X-rays then being attenutated (blocked) by the actual electric circuitry of the cassette itself (for easy of use, weight, etc, there is no shielding on DR cassette to block those X-rays coming from the wrong direction while there is on plain film and CR cassettes - so yes, if you see backscatter, you are using DR rather than CR or film-screen radiography).
 
So how can you correct for this?

• Decrease your mAs (ie drop the amount of X-rays used)
• Collimate better so more of the X-rays are focused on the detector
• Add lead backing to the cassette

Again, this is just one of the MANY type of radiographic imaging artifacts. For anyone learning or just interested, check out the Radiopaedia link above or Radiographics has a fairly good review article here:

@RadioGraphics

Visual familiarity with the variety of digital radiographic artifacts is needed to identify, resolve, or prevent image artifacts from creating issues with patient imaging. Because the mechanism for image creation is different between flat-panel detectors and computed radiography, the causes and appe…

RadioGraphicsAlisa I. Walz-Flannigan

History: Hand/Wrist Pain

Answer:

Rheumatoid Arthritis (Wrist)

Rheumatoid arthritis is a chronic autoimmune inflammatory disorder that affects numerous organs, the most classic of which are joints and synovial soft tissues.
 

• overal prevalence of ~1% of the population
• onset typically in 4th- 5th decade of life
• 2-3x's more common in females
   

It is theorized that through a combination of genetic predisposition (HLA-DR B1 allele) and some environmental trigger (Ebstein-Barr virus is thought to play a role), the body initiates an autoimmune response. IL4, TNF, and B-cells produce Rheumatoid Factor antibodies against natural IgG yielding immune complexes that are deposited through the body. This response attacks numerous organ systems such as the skin, heart, lungs, and classically the joints of the musculoskeletal system.
 
For this brief write-up, I am going to focus primarily on the articular manifestations of RA.
 

• Inflammation -> pannus formation (ie thickened, hyperplastic synovium)
• Pannus contains granulaton tissue including lymphyocytes, plasmacytes, macrophages and osteoclasts
• The pannus slowly destroys the articular cartilage, however the "bare areas", which are the small areas of exposed bone peripheral to the cartliage but still contained within the joint space (see image below), are less protected than the cartilage and show destructive changes much earlier.

Clinical Presentation (MSK):

• Onset can be slow or rapid
• Inflammatory appearance: warm, painful, swollen and stiff joints with limited range of motion

Radiology

Radiography:

• Marginal erosions - ie at the "bare areas" we described above (it seems to favor the radial side of the metacarpophalangeal joints). As it progresses, the pannus/inflammation evidentually errodes through the articular cartilage to get more diffuse erosions and subchondral cyst formation (fluid extending into the bone through areas of articular/cortical destruction)
• Joint space loss - typically concentric and symmetrical
• Osteoporosis - inflammation yields hyperemia about the joints -> increased bone resorption in a periarticular distribution
• Soft tissue swelling - inflammation -> edema about the involved joints

Hand/Wrist Specifics:

• RA involves the more proximal joints of the wrist and hand such as the intercarpal, MCP (especially 2nd and 3rd), and PIP joints and typically spares the DIP joints
• Ulnar styloid is a classic site of erosion in RA
• Late Stage changes:
  • carpal instability and SLAC wrist (scapholunate advanced collapse)
  • hitchiker's thumb deformity (flexion of 1st MCP and hyperextension of 1st PIP joint)
  • joint anylosis
  • joint subluxation (ulnar deviation at MCP joints, boutonniere deformity and swan-neck deformity)
  • pencil-in-cup deformity (classically taught as characteristic of psoriatic arthritis, it also commonly occurs in RA)
  • scallop sign (erosion of the radius at the distal radial ulnar joint - though to prelude extensor tendon rupture)

Other Imaging Modalities

Ultrasound

• Ultrasound can be an early diagnostic tool in articular assessment of RA by examining the synovium itself. Even before bone destruction you can see:
  • synovial thickening/hypertrophy
  • synovial hyperemia
  • bursitis
  • tenosynovitis - ie fluid and inflammation involving the tendon sheath (classic is the extensor carpi ulnaris tendon)

And Ultrasound can even be useful for interarticular steroid injectons as treatment.

MRI

• MRI is very sensitive to similar findings above
  • synovial thickening (shedding of pieces of synovium -> rice bodies)
  • synovial hyperemia
  • pannus formation
  • subchondral edema, csyts and erosions
  • cartliage thinning/destruction

as well as:

• joint effusions
• periarticular marrow edema (ie osteoclastic activity and osteopenia)

Summary (TLDR)

• Rheumatoid is an INFLAMMATORY process affecting joints
• Clinical symptoms of inflammation (swelling, redness, pain)
• Pannus affects "bare areas" so periarticular erosions/destruction (note the lack of productive change till superimposed osteoarthritis develops
• Wrist is classic joint for involvement, affecting the proximal joints (intercarpal, MCP, PIP) versus OA being more wear phenomenon affecting distal joints
• Classic ares of involement:
  • ulnar styloid erosions
  • 2nd and 3rd MCP joint erosions
  • triquetral erosions

A common problem is that everyone seems to want to call everything "degenerative", ie osteoarthritis. As we've already stated, osteoarthritis is a mechanical wear phenomenon. Essentially the cartliage just wears down. Since bone doesn't particularly like to rub against other bone, and really the only thing bone can do is make more bone, it uses productive processes to reinforce the cortex (subchondral sclerosis) while bridging the joint to minimize further wear (osteophytes limiting joint motion).

If you are confusedm, here is a table I made up to help differentiate between the two:

Our Patient

Here we have a 61 yo female with 2 months of worsing atraumatic wrist and hand pain.

Radiographic Findings:

• Diffuse intercarpal joint space loss and carpal/ulnar styloid erosions (blue arrows). Note the large subchondral cyst in the distal radius (long blue arrow)
• radiocarpal joint space loss (light green arrows) with proximal migration of the capitate (dark green arrow) consistent with developing SLAC wrist
• scalloping of the radial aspect of the Distal radial ulnar joint (red arrow)
• soft tissue swelling over the ulnar styloid consistent with tenosynovisits of the extensor carpi ulnaris tendon (yellow arrows)

History: Trauma. Abdominal pain.

Do you see anything? Any other imaging requested?

Would you like more images?

There was no free fluid within the abdomen and the rest of the abdominal structures were normal. How does this affect your impression?

Answer:

Focal Nodular Hyperplasia (FNH)

Did you know that the liver is the only self-regenerating internal organ in the human body?

Focal nodular hyperplasia is a result of this regenerative capacity, where there is proliferation of hepatocytes with abnormal vascular supply, vascular drainage and biliary drainage. This response is believed to be secondary to areas of hypo- or hyperperfusion, and thus current thought is that the presence of underlying arterial malformations can play a major role in development (note the increased incidence of FNH with Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia as well as with hepatic hemangiomas). Arterial supply is generally from the hepatic artery and venous drainge is through the hepatic vein (ie NO portal venous connection).

• FNH is a benign condition, and is the second most common benign hepatic lesion behind hepatic hemagiomas
• Most commonly found in young to middle-aged adults
• 5-6x's more common in females
• Solitary most common but 20% multifocal
• 25% seen with other vascular pathologies such as hemangiomas, AVMs, Budd-Chiari syndrome (hepatic venous obstruction), portal shunts, Osler-Weber-Rendu, etc
  
  

Types:

• Typical

  • poorly encapsulated large mass (4-8cm)
  • prominent central scar with radiating fibrous septae (~50% of cases) forming a pseudocapsule***
  • prominent central artery with spoke-wheel configuration
  • abnormal cellular architecture but can contain bile ducts and Kupffer cells (reitculoendothelial hepatic macrophages)

• Atypical

  • lacks central scar and central artery (makes diagnosis difficult)
    
    

Radiology

Ultrasound:

• variable echogenicity of both the lesion and central scar
• may be isoechoic to hepatic parenchyma and thus not seen
• sometimes can see the spoke-wheel vascularity

Multiphasic CT:

• Non-contrast: hypo- or iso-attenuating (or hyper attenuating in a low density fatty liver)

• Arterial: bright homogeneous arterial enhancement EXCEPT central scar
  Portal Venous: washout yielding iso-hypoenhancing to liver (often difficult to even see)

• Delayed: central scar can demonstrate delayed ehancement (80%)

• macroscopic fat, calcification and hemorrhage are not typical findings

MRI:

• T1: iso- to moderate hypointense, hypointense scar
• T2: iso- to hyperintense, HYPERintense scar
• T1 +c (Gd): intense early arterial enhancement, washout to isointense portal venous phase, persistent enhancement of scar on delayed phase
   
  Alternate contrast agents:
• Eovist/Primovist: washout is less than Gd so mild enhancement persists on delayed imaging (vs adenomas which are hypointense on delayed sequences)
• SPIO: a reticuloendothelial agent, ie taken up by Kupffer cells (see nuclear medicine below) -> hypointensity due to suscpetibility signal loss (again vs adenomas which have less to no Kupffer cells)

Nuclear Medicine:

Tc-99m Sulfur colloid is the classic radiotracer used for diagnosis. Similar to SPIO above, sulfur colloid is taken up by the reticuloendothelial system, ie the Kupffer cells, and thus it can distinguish FNH from other lesions that do not contain normal parenchymal elements. Classically FNH is "hot" (Hincreased radiotracer uptake) versus other lesions which should be "cold" (photopenic or low uptake) within the normal low level normal hepatic uptake.
 
Tc-99m HIDA exam should show the same uptake as normal liver. Since HIDA is taken up by hepatocytes and excreted in the biliary system, and FNH contains all the normal cells and bile ducts, it should appear background to "hot" just like the contrast agents above.

Our Patient

I presented the case a bit backwards for teaching purposes.
 
On the left we have the arterial phase. Note the rounded area of early enhancement anterior to the IVC, even showing a linear, low density central scar.
 
On the right we have the portal venous phase. Here we can see the normalization of the enhancement so it now is the same as the remaining liver, but we can still make out that linear, low density central scar.
 
Given the way I presented it and the history of trauma (which was the real history), laceration should definitely been up there on the differential. But given the arterial imaging, and lack of secondary traumatic findings, the appearance is most consitent with benign focal nodular hyperplasia

History: Chest Pain

Answer:

Answer: Lipomatous hypertrophy of the interatrial septum

This entity is exactly what the name implies, there is hypertrophy and fat deposition between the fibers of the inter-atrial septum.

• Commonly has a smooth mass-like bulge into the atrium
• usually spares the fossa ovalis (the "closed" depression in the right atrium at the site of a formerly patent foramen ovale during fetal development)
• Does NOT have a capsule (cardiac lipomas do have a capsule)
• associated with mediastinal lipomatosis (excess fat deposition through the mediastinum)

Radiology:

Plain films: not appreciated (perhaps an enlarged mediastinum if there is associated diffuse lipomatosis)

CT: thickened (>2cm), nonenhancing fat (very low) density between the right and left atria. Again, commonly spares fossa ovalis yielding a bilobed or "dumbbell" appearance.

MRI: high intensity on T1, hight= intensity on T2, low intensity on fat-suppressed consitent with fat. Should be homogeneous.

PET: shows + FDG uptake theorized due to brown adipose fat composition (remember, brown fat is FDG avid).

Clinical:

Generally this is a benign and incidental finding and no further work-up or treatement is necessary unless there is significant mass effect on SVC or atrium.

But this has been associated with cardiac dysrhythmias (eg atrial fibrillation, premature atrial contractions and atrioventricular block) as well as syncope and sudden death. So in the setting of cardiac conduction abnormalities, perhaps one may want to suggest Cardiology consultation.

This Patient

In this patient, it was believed their pain was due to an alternate etiology so no further work-up was felt warranted.

The key is to recognize this and differentiate from other cardiac lesions such as:

• cardiac lipoma (usually more capsulated, extraluminal)
• cardiac rhabdomyoma/rhabsomyosarcoma (usually more pedunculated intraluminal lesions, think ventricular, often with calcifications from prior intra-lesion hemorrhage. + enhancement, usually in newborns/very young pts)
• atrial thrombus (purely intra-luminal)
• cardiac myxoma (usually Left atrial, low but not fat density, can have calcification, often move with contraction)

History: Trauma

Can you name the body part and the diagnosis?

Answer:

Testicular Fracture

As the name implies, this is a traumatic tear to the parenchyma of the testicle. This is often associated with rupture of the tunica albuginea (as show above).

Radiology

Ultrasound is the key diagnostic modality in examination of the scrotum and testicles.

• Hypoechoic line or parenchyma within the testicle (similar to an organ laceration on CT)
• Contour irregularity of the testicle
• Closely examine vascularity of all portions of the testicle, looking for areas of devascularization (remember the whole testicle doesn't have to be devascularized)
• Look for an associated complex hydrocoele (ie hematocoele) and other injuries - don't forget to perform a careful examination of the contralateral testicle also!

Treatment/Progrosis

• Prompt surgical consultation and imaging to assess for viability.
• Treatment can range from debridement to resection depending on degree of injury and amount of viable (vascular) tissue remaining

Our Patient

These images show marked contour abnormality of the right testicle consistent with tunica albuginea rupture and fracture of the parenchyma with extrusion of the parenchyma beyond the capsule (ie area so graciously surrounded by areas by the technologist). This same area is very heterogeneous in echotexture with essentially absent vascular flow on both color Doppler (left images) and Power with M-mode (bottom right).

Above left images better demonstrates the extruded testicular parenchyma beyond the tunica, almost surrounding the epididymus (calipers).

Above right images shows the hematocoele (ie clot/complex fluid) around the testicle.

While rare, these do certainly occur, and prompt diagnosis and treatment is key to minimizing morbity.

Hx: 27 yo with Shortness of Breath

Answer:

Multiple Answers:

1. Swyer-James Syndrome of the Right Lung
2. Small right apical pneumothorax

Swyer-James Syndrome

• aka Swyer-James-Macleod Syndrome, Bret Syndrome, hyperlucent-lung syndrome

• a rare condition typically involving unilateral, lobar or even segmental hypoplasia of the pulmonary vasculature with air-trapping and +/- bronchiectasis

• Classically the result of postinfectious obliterative bronchiolitis from viral infection or Mycoplasma pneumoniae infection in early childhood

Radiology

Plain Films

• Hyperlucent lung can be entire lung, lobar or smaller, with dimished vasculature.
• Air-trapping on expiration

CT

• Better visualization air-trapping (hyperlucent lung parenchyma) with decreased vascularity
• Involves entire lung or even can be patchy subsegmental distribution
• Typically, areas of involvement are smaller in volume than the normal lung -> decreased size of that hemithorax
• +/- bronchiectasis/bronchial wall thickening

Nuclear Medicine

• Photopenic areas on V/Q imaging

MRI

• Generally not good at lung parenchyma evaluation
• Can show a small pulmonary artery and fewer peripheral arteries

Prognosis/Treatment

• Generally very good prognosis. Commonly diagnosed incidentally later in life
• This can predispose to recurrent infections
• Controversy over whether steroid use is helpful

Our Patient

While the right hemithorax is not necessarily smaller than the left, it is definitely hyperlucent. And note the signficiantly diminished vascular markings on the right versus the left.

Oh yeah, and there is just happens to be an irregularly shaped (versus multiple) lucency in the right pulmonary apex. Bullae? Scarring? Pneumothorax?

CT from the same patient shows:

1. Hyperlucent areas throughout the right lung, especially the RUL (axials - top row) and posterior RLL (coronals - bottom row)
2. Bronchiectasis and bronchial wall thickening most prominent in the RUL
3. Diminished vascularity throughout much of the right lung when compared to the left
4. Definite pleural air (ie pneumothorax) in the right pulmonary apex with areas of scarring extending from the visceral to parietal pleura. Could this be chronic?

While our patient may not demonstrate the classic "small" lung, it does show the unilateral hyperlucent lung (CXR) and regional areas of hyperlucency/air-trapping with associated dimished vascularity and bronchiectasis consistent with Swyer-James Syndrome.

Oh yeah, and a right apical pneumothorax!

Do you want to see additional causes of Unilateral Hyperlucent lung?

Check out:

Season 10 Case 6

The Chest X-ray game. Same finding. Can you find the cause on each?

WetreadWetreadRad

History: 2 week follow-up post surgery. What is the important finding? Can you tell what type of surgery this patient underwent?

Answer:

Answer: Pneumatosis coli status post bilateral orthotopic lung transplant (BOLT)

While the specific surgery may or may not be important (we'll get to that later), you can clearly see the surgical clips over both hilar regions, the extensive mediastinal wires and the bilateral cutaneous staples. This is consistent with a bilateral lung transplant.


More importantly, did you see the finding in the abdomen?

There is extensive air/pneumatosis involving the colon. While the abdominal view does a good job showing the extensive gas in the wall of the ascending colon, the upright chest X-ray demonstrates it well in the splenic flexure.


Want a better look?

Pneumatosis coli

Pneumatosis coli is the term used to describe the appearance of intramural gas within the colonic wall. When it is the small bowel that is involved it is termed pneumatosis intestinalis. When it has a more cystic appearance, the term cystoides can be added to either version.

Pathologic composition of the gas depends on the etiology.

Etiology

Divided into 2 groups:

Benign:

• Pulmonary disease (asthma, emphysema, cystic fibrosis, etc)
• iatrogenic/procedural (ex jejunostomy tube placement, endoscopy)
• systemic diseases (lupus, scleroderma, AIDS)
• medications (corticosteroids, chemotherapy, lactulose)
• organ transplantation
• Primary pneumatosis- idiopathic, generally involves the colon with cystic air collections (= penumatosis cystoides coli/intestinalis)
  
  

Life-threatening:

• Intestinal ischemia
• intestinal obstruction (esp strangulation)
• enteritis/colitis (ex necrotizing enterocolitis in newborns)
• toxic megacolon
• trauma
• organ transplantation (particularly bone marrow transplant and graft-versus-host disease)

Treatment

• Depends on underlying etiology
• Correlate for any pertinent history (above) and with clinical status - ie pain, surgical abdomen
• For benign causes, simple gut rest can be sufficient
• Lab values can be helpful (serum lactate)
• CT can be very helpful to look for life-threatening etiologies, ie
  • bowel wall thickening or abnormal enhancement (bad)
  • more linear air collections tend to be more concerning
  • portal venous gas (very bad)
  • mesenteric arterial/venous thrombosis (bad)

Complications:

• Pneumoperitoneum can occur from rupture into the peritoneal cavity. Treatment still is generally based upon the causative etiology.

Our Patient:

As you've probably put together by now, this patient had undergone a bilateral orthotopic lung transplant and this was chest X-ray was performed as part of their routine follow-up. We noted above that organ transplantation is one of the known causes of benign pneumatosis coli and it seems lung transplants are a relatively common example. The vast majority of these patients seem to be of the benign type and do well with gut rest and sometimes steroids (which ironically is the major drug induced cause), but CMV colitis can be a common opportunistic infection in lung transplant recipients so consideration for antivirals may be warranted.


Our patient did fine with monitoring and had no real symptoms or issues with it improving over the next few days.

References:

• Ho LM, Paulson EK, Thompson WM. Pneumatosis intestinalis in the adult: benign to life-threatening causes. AJR Am J Roentgenol. 2007 Jun;188(6):1604-13. doi: 10.2214/AJR.06.1309. PMID: 17515383. https://www.ajronline.org/doi/pdf/10.2214/AJR.06.1309
• Chandola R, Laing B, Lien D, Mullen J. Pneumatosis Intestinalis and Its Association With Lung Transplant: Alberta Experience. Exp Clin Transplant. 2018 Feb;16(1):75-80. doi: 10.6002/ect.2016.0289. Epub 2017 Oct 31. PMID: 29108518. https://pubmed.ncbi.nlm.nih.gov/29108518/

History: Knee Pain

Do any names come to mind?  Are the findings related to the patient's current pain?

Answer:

Answer:

1) Sequela of prior Osgood-Schlatter's disease

2) Sequela of prior Sinding-Larsen-Johansson disease

Osgood-Schlatter's disease

• a fatigue or traction injury of the distal patellar tendon at it's insertion on the tibial tubercle
• usually due to recurrent microtrauma
• classically affects boys 10-15 years old (particularly those with frequent jumping or kicking)
  
  

At presentation there is focal pain at the tibial tubercle. Presentation is almost always pathognomonic so imaging is not often performed.


Radiographs can show focal soft tissue swelling over the tibial tubercle. After about 3-4 wks of healing is when the classic small ossifications/ fragmentations develop, which can persists indefinitely.


MRI of acute disease shows a thickened, edematous distal patellar tendon with pre-tibial soft tissue edema. +/- underlying bone edema or associated infrapatellar bursitis.


Treatment is conservative with rest, ice, limiting activity and antiinflammatory medicines.

Sinding-Larsen-Johansson disease

• essentially the same pathology as above but affecting the patellar tendon origin from the inferior patella
• again, classically affects boys 10-14 years old (also associated with jumping/kicking)
  
  

Presentation is focal pain/swelling at the inferior pole of the patella, and again is fairly pathognomonic in this age group (very similar to the pathology of "Jumper's knee" which is seen at all ages).


Radiographs can show focal soft tissues swelling over the inferior pole of the patella. Sometimes one is able to make out thickening of the proximal patellar tendon with stranding anterior and/or posterior to the tendon. Over time you can get fragmentation/small ossification of the proximal tendon (similar to Osgood-Schlatter's), or enthesophyte formation.


MRI/US of acute disease will show thickening and edema within the proximal patellar tendon +/- inferior patellar bone edema.


Again, treatment is conservative with rest, ice, limiting activity and antiinflammatory medicines.

Our case

The green arrow shows the sequela of Sinding-Larsen-Johansson, ie fragmentation/enthesopathy formation of the lower pole of the patella.


The blue arrow shows sequela of Osgood-Schlatter's disease with fragmentation/ossification in the distal patellar tendon.


Note that there is no significant soft tissue swelling at either site. Additionally it is pretty obvious that this patient has fused growth plates which puts them out of the realm for either of these syndromes. So these changes are NOT ACUTE. Rather, they presumably had both syndromes as an adolescent and these are the benign changes that persisted.


The key to remember is that these changes are not those of acute disease, rather, as makes sense, the calcification is a typical part of the healing process. Similar processes take place at:

• triceps tendon insertion on the olecranon
• biceps tendon insertion on the radial tuberosity
• Achilles tendon insertion on the posterior calcaneous
• plantar fascia origin of the inferior calcaneous
  
  

So if you mention them for an adult, make sure you specify that these are remote or chronic findings.

Just of interest, would you like to see the contralateral side?

History: Head and neck pain. No history of trauma

Would you like more images?

Answer:

Answer: Basilar Invagination

Basilar invagination is when the tip of the odontoid process extends above the foramen magnum into the cranial vault. This yields narrowing/stenosis of the foramen magnum and thus mass effect/compression of the medulla or upper spinal cord. This results in:

• obstructive hydrocephalus
• neurologic symptoms of compression of the brainstem/spinal cord
• syringomelia
• even death if severe

Note: basilar invagination and basilar impression are similar terms but not identical. Basilar impression specifically refers to when there is invagination due to "settling" or "softening" of the skull base without other identifiable cause. Both can yield the same symptoms.

Etiology

Congenital:

• Chiari I/II malformations
• osteogenesis imperfecta
• Achondroplasia
• rarer entities such as Klippel-Feil syndrome or cleidocranial dysostosis
  
  
  Acquired:
• Rheumatoid arthritis (can be seen in up to 10% of RA patients)
• Osteomalacia/rickets
• Paget's disease
• Hyperparathyroidism
• Trauma

Radiology

Diagnosis of basilar invagination relies on the classic 5 lines on plain films or reconstructed CT:

Lateral view:

• McRae's line: tip of basion to opisthion (tip of odontoid should be 100% below this line)
• Chamberlain's line: posterior point of hard palate to opisthion (tip of odontoid should be <3mm below this line)
• McGregor's line: posterior point of hard palate to most caudel point of the occipital condyles (tip of odontoid should be <5mm above this line)

Basion = posterior, inferior tip of the clivus
Opisthion = most posterior margin of the foramen magnum at midline

Frontal View

• Digastric line - between the bilateral digastric grooves (odontoid should be 11-21mm below this line)
• Bimastoid line - between inferior points of mastoid processes (odontoid should not extend >10mm above this line)

Our Patient

I actually went easy on you. The only real history in this case was "headache". No neck pain reported. No CT C-spine ordered. This was an incidental finding. Do you happen to see why?

Notice that C1 is actually completely collapsed and fragmented on the left. This is both causing the malalignment at the right atlantooccipital joint, but also causing the dens to protrude upward through the foramen magnum.

Unfortunately this patient had known metastatic breast cancer so here we have a pathologic fracture with complete collapse/flattening ("plana" deformity) of the left lateral mass of C1.

I will admit, I am not the biggest fan of memorizing numbers. In this situation I tend to rely much more upon McRae's line since that is a much more binary decision. If the odontoid tip goes above the line = BAD. If it goes to the line, maybe that's when I get out my ruler... maybe :)

What is going on here? And is it normal or abnormal?

History: skateboard injury to perineum

Answer:

Answer: Retrograde Urethrogram (RUG) with injury to the bulbous urethra

First we should go a bit into the anatomy of the urethra

We are focusing on male anatomy because female urethral anatomy is much less complex and much less commonly injured

Anatomy:

There are 4 major parts of the male urethra:

Posterior Urethra

1. Prostatic urethra (obviously portion within the prostate)
2. Membranous urethra (portion below the prostate extending to the urogenital diaphragm)
   
   

Anterior Urethra
3. Bulbous (bulbar) urethra (U-G diaphragm to base of penis)
4. Penile urethra

Mechanism of Injury

Most common injury is from pelvic fractures yielding injury to the posterior urethra. This can be associated with bladder injury.

Straddle injuries are the next most common and tend to yield direct trauma to the perineum and anterior urethra, often compressing it against the pubis.

Clinically look for:

• Hematuria
• Blood at the urethral meatus
• evidence of trauma - swelling/bruising/hematoma
• inability to void

Procedure Technique (Retrograde urethrography)

This is not a very common procedure for Radiologists these days. The premise is simple, fill the urethra up with contrast, but it can be a bit tricky. Here are some tips:

1. Positioning is key - have the patient roll ~30degrees towards you and gently lengthen out the urethra as much as possible
2. minimally lubricate the catheter and insert it ~2-3cm into the urethral meatus. There is a small outpouching just proximal to the meatus called the fossa navicularis, which is ideal position of the catether tip
3. Personally, I forgo clamps and insulflation of Foley bulb and just have the patient use his fingers to effectively clamp the Foley just proximal to the meatus (warning - too much lubrication can cause the catheter to squeeze out during injection. If you let the patient know this they can be your best friend by squeezing as tight as the can tolerate. And that way you don't have to re-insert and get it done ASAP.)
4. Inject your water soluble contrast retrograde to fill the penile and bulbous urethra. It can take a bit of pressure with injection to get contrast beyond the U-G diaphragm, but often you can get it retrograde all the way into the bladder (again with a helpful patient to prevent backpressure forcing the catheter out).
   
   

In a trauma situation, you can either do a RUG or an antegrade urethrogram (essentially image urination after contrast is installed in the urinary bladder. This can often visualize the posterior urethra much easier assuming the patient is able to perform such a procedure.

Grading Systems

There are 2 grading systems for urethral injuries:

AAST injury scale

Goldman classification

Our Case

In our case, this individual was skateboarding and had an unfortunate straddle injury landing on his skateboard. He had pain and blood at the meatus.

The blue arrow above shows extravastion from the bulbous urethra consistent with a Goldman Class 5 injury if you want to classify it. Much of the AAST and Goldman are focused on posterior urethral injuries which we don't have here. The brisk extravasation limited the ability to get contrast past the U-G diaphragm but we were more focued on an anterior injury anyway given the history and symptoms.

The yellow arrow is the penoscrotal junction, where the suspensory ligament attaches. You can commonly see narrowing here dependent on positioning of the penis (also likely exaggerated by foreshortening of the penile urethra due to positioning). This should distend well with good positioning and a good injection.

There are several non-traumatic reasons for performance of urethrography including:

• stricture (eg post-infectious, prior instrumentation, prior trauma, etc)
• diverticulum
• urethral tumors
• fistuals
• foreign bodies

Reference:

Excellent Radiographics article on urethral injuries as previously mentioned:

Ingram MD, Watson SG, Skippage PL, Patel U. Urethral injuries after pelvic trauma: evaluation with urethrography. Radiographics. 2008 Oct;28(6):1631-43. doi: 10.1148/rg.286085501. PMID: 18936026. https://doi.org/10.1148/rg.286085501