#season08

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Case 35

History: neck and check pain. Swelling

Answer: Thrombophlebitis of the Left bracheocephalic vein with mediastinitis

Check out the new X-ray. We definitely see widening of the upper mediastinum. But can we be more specific? Where is the “mass”

We can see from our current exam that the contour of the aortic silhouette (red arrow) is maintained so it should not be adjacent to the aorta. If fact it actually obscures the left subclavianartery silhouette (yellow arrows) so it has to be in that region of the anterior mediastinum.

So what’s next? How about the CT?

 Now we clearly see the extensive stranding throughout the anterior mediastinal fat, with severe narrowing of the left bracheocephalic vein and left jugular vein.

Finally we have the Doppler Ultrasound of the left jugular vein showing occlusion. In fact the left jugular and subclavian veins were thrombosed as centrally as able to be visualized.

What’s the source? Here’s a higher slice from the neck CT showing retropharengeal fluid likely relating to pharengeal infection.

In summary, we have thrombosis of the left jugular, subclavian and bracheocephalic veins with associated thrombophlebitis and mediastinitis preumably secondary to a pharyngeal infection.  This is similar to a Lemierre’s Syndrome however classically that involved the internal jugular vein but here we have common jugular and distal thrombophlebitis.

Lemierre’s Syndrome:

Presentation: 

Neck pain and swelling with ongoing/recent oropharengeal inection

Male predominance

generally 16-25 years old

Pathology:

80% caused by Gram (-) Fusobacterium necrophorum but can get polymicrobial even including MRSA

Radiology:

shows jugular vein thrombosis. US generally easiest and most straight forward but can be limited in the chest

CT/MR can be helpful for more central venous evaluation and to identify source/site of primary infection

Complications: Pulmonary Septic emboli and systemic dissemination

Treatment: Anticoagulation and IV Abx. Mortality rates can be as high at 18%.

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Wetread Case 40 Answer

History: elbow swelling

Answer: Olecranon Bursitis secondary to Gout

Obviously we have focal mass-like soft tissue swelling posterior to the olecranon with minimal soft tissue edema otherwise about the elbow. This is classic picture of olecranon bursitis

Etiologies for olecranon bursitis:

-trauma

-excessive use (aka “student’s elbow” or “baker’s” or Popeye elbow) 

-infection

-inflammation (classically gout, although RA and CPPD as well)

In this case we also see soft tissue Ca++ which we wouldn’t expect to see in trauma or overuse but can be seen with gout. 

The issue that often comes up by inexperienced clinicians is concern for infection and desire to aspirate (heck just google “OB” and one of the first pics has a needle). I highly suggest you DO NO ASPIRATE. Gouty OB can be swollen, tender even mildly red/warm due to the inflammation. But if it isn’t infected when you tap it, it will be afterwards. And an infected bursa can be extremely difficult to treat with Abx and might even require surgical removal.

This is not an uncommon findings and almost always due to overuse or gout/RA.So keep the needle away!

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Season 8 Case 39

History: altered mental status

Answer: Psuedosubarachnoid hemorrhage secondary to hypoxicischemic brain injury

In these 2 images we see hyperdensity (increased attenuation) along the basilar cisterns. While this is a common appearance of subarachnoid hemorrhage secondary to Circle of Willis Aneurysm rupture, we need to look at the entire image and the entire exam!

How about the basilar cisterns? - They are effaced

How about the grey-white junction?  - It is gone.   In fact, Normally grey matter is slightly hyperdense compared to the white matter, but here we have the peripheral grey matter actually lower in density than the central white matter (aka the reversal sign)

How about the central grey matter structures?  Similarly, the caudate nuclei, basal ganglia and even thalami are all low in density - which again is not normal

How about the normal sulcal pattern of the cerebrum?  - It’s gone. In fact can you even find a sulcus? (and the patient isn’t 15 years old)

This is an example of global anoxic injury aka hypoxic-ischemic encephalopathy. Global anoxia leads to neuron injury. Since grey matter is more metabolic than white matter, it is effected earlier and more severely. Anoxia/Ischemic -> neuron injury -> edema -> decreasing grey matter density.

So what about that increased density all throughout the basilar cisterns, sylvian fissure, falx and tentorium?  While it may look like blood, it’s actually artifact - ie pseudosubarachnoid hemorrhage. 

Because of the cerebral edema, particularly the grey matter edema, the parenchymal density decreases. This combined with outflow venous dilation and thrombosis secondary to the increasing intracranial pressure, yields the appearance of increased density particularly throughout the basilar cisterns. 

If you can get a good density measurement you will see it is more in the normal 30-40 HU venous density range compared to extra-vascular or true subarachnoid hemorrhage in the 60-70 HU range.

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Wetread Case 38

History: chest pain

Diagnosis?

Answer: Penetrating Atheromatous Ulcer (PAU)

What? How you say? Let’s walk through this.

Here’s the current Chest X-ray and I’ve added labels (blue = heart border, red = aorta, orange = hilar vessels). 

We see a left infrahilar mass that doesn’t obscure the left hear border (blue) but does obscure the aortic border (red, with dashed lines being where we think it should go and the dark red line outlining the mass). We can still see the hilar vessels (orange) so this mass can not be the vessels nor silhouette the vessels (ie the hilum overlay sign)

So this mass has to either obscure the border of the descending thoracic aorta or be the descending thoracic aorta. And if it is the aorta, we have a focal mass or enlargement of the aorta. 

Can we confirm?

It is difficult to see the entire aorta, but red lines are my guestimate suggesting increased diameter over the mid throacic spine.

So when the answer box (aka CT scanner) comes back up, here is what we see.

Sure enough there we see focal bulging of the aorta which just so happens to contain contrast in keeping with a PAU.

Aortic wall pathology can be a bit confusing. There are a bunch of good articles including Radiology Assistant  from which I am borrowing their wonderful images. I encourage everyone to go read their wonderful write-up. In summary:

Intramural hematoma is isolated blood within the vessel wall with no connection to the inner lumen

Ulcerated plaque is just that, an ulcer in atheromatous plaque but it does NOT extend beyond the intimal layer

If the ulceration errodes beyond the normal intimal layer into the vessel wall (ie the media layer), now we have a penetrating atheromatous ulcer (PAU)

All of the above can progress to an aortic dissection. So there is injury to the vessel intima allowing blood into the media layer and then the pressure gradient causes extension of the injury through the vessel wall (ie media layer)

While that may be a bit simplistic, hopefully that helps understand the different types of aortic wall pathology.

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Season 8 Case 37

History: Abdominal pain. Palpable mass

Answer: De Garengeot Hernia with acute appendicitis!

A De Garengeot hernia is a femoral hernia containing the appendix, which is exactly what we have here but the appendix is hyperenhancing with wall thickening and surrounding fluid consistent with acute appendicitis.

Named after a French surgeon from the 1700s, these are fairly rare (<3% of femoral hernias), with complicating appendicitis even more rare.

Understanding groin hernias can take time and they are not always easy to figure out. There are 2 major types:

Inguinal hernia

~80% of abdominal wall hernias

MLF ratio of 7:1

Types:

1) Indirect 

-more common

-Can be a)congenital defect in a patent process vaginalis in young males or b) acquired do to stretching/weakness of the inguinal ring in older patients

- passes through deep inguinal ring 

- LATERAL to the inferior epigastric artery

- anterior to spermatic cord or may insinuate around the inguinal contents

2) Direct

- less common

- secondary to weakness in floor of inguinal canal (Hesselbach’s triangle)

- MEDIAL to inferior epigastric artery (therefore inguinal contents generally displaced laterally)

Image below shows the inferior epigastric vessels labeled as Orange so the fat lateral to the vessels would be the INDIRECT hernia (blue) and the fat medial the the vessels (red) would be the DIRECT hernia.But both go into the inguinal canal, just through different routes.

A femoral hernia is a hernia through the femoral ring, so it is inferior to inguinal ligament and lateral to the inguinal canal. As it protrudes through the femoral ring, it can compress the normal femoral canal contents, primarily the femoral vein. You tend to see it seeing more on top of the pectineus muscle as it lies on the superior pubic ramus.

Here we see a small fat containing femoral hernia (yellow) compared to a normal inguinal canal (blue)

Groin hernia summary: Inguinal hernia extend inf and medial into inguinal canal. Direct take a "direct course" medial to inf epigastric artery vs Indirect go more "indirectly" lateral to vessels Femoral hernias go inf and lateral through femoral ring compressing the femoral vein. 

"Fancy" Groin hernias: 

 Amyand hernia = inguinal hernia containing appendix (some say specifically appendicitis) 

 De Garengeot hernia = femoral hernia containing appendix (or appendicitis as we see here!) 

Here we have a De Garengeot Hernia. Labels: Hernia yellow, appendix red 

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Wetread Case 36

History: wrist pain

Answer: Dorsal Intercalated Segment Instability (DISI)

So what findings do we see:

1) Widened scapholunate distance =Injury to the S-L ligament yields widening of the distance, commonly referred to as the Terry Thomas sign (or for younger Rads the David Letterman Sign, the Madonna Sign, or the Michael Strahan Sign)

2) Abnormal scaphoid - Note the scaphoid’s appearance on the frontal exam. The radial margin is not normal consistent with a prior fracture deformity. Since scaphoid fracture is the most common carpal fracture, it makes sense a single injury could cause both the fracture and the S-L ligament injury

But what about the lateral  exam?

3) Dorsal rotation of the lunate bone

The carpal bones and their ligaments have a complex relationship. Primarily the proximal and distal rows form a kind of “ring”. However, there is a three dimensional twist or torque to that ring. What that means is that when the is disruption of the ring, such as by complete tearing of the scapholunate ligament, not only does the ring widen, but the bones are allowed to “un-torque” or untwist. 

When this happens the scaphoid will start rotating volarly (towards the palm) and the triquetrum/pisiform will start rotating dorsal (to the back of the hand). The lunate goes along with whichever it is connected to. And since we have torn the Scapholunate ligament, it rotates with the triquetrum dorsally - ie DORSAL intercalated segment instability.

Interestingly, if instead you tear your lunotriquetral ligament, the lunate will then rotate with the scaphoid towards the palm (volarly) = VOLAR intercalated segment instability (VISI)

Orthopedics like measuring things so you can measure:

scapholunate angle (nl 30-60)

capitolunate angle (nl <30) 

radiolunate angle (nl <15). 

 Here I drew in the bone outlines and measured the capitolunate angle which is >30 degrees (ie the dorsal tilt of the lunate) 

Generally these findings can be seen on X-ray. You can measure the S-L distance (nl <2-3) but it does vary upon gender. Generally >3mm abnl If you want fancy pictures you can do an MRI to look for bone contusions or even an MR Arthrogram to eval the  S-L ligament directly.

Clinically:

 - Radial/dorsal wrist pain, esp w radial deviation or extension 

- weakness/instability 

Concurrently, as the bones are “untwisting”, you will get abnormal wear and osteoarthritis at the radioscaphoid joint and the capitate bone will gradually migrate proximally to fill the scaphol-lunate interval. This is termed Scapholunate Advance Collapse (SLAC wrist)

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Case 34 Answer

History: palpable mass

Answer: Calcinosis of Chronic Renal Failure (ie secondary tumoral calcinosis)

The exact name of this is somewhat confusing. True Tumoral Calcinosis (TC) is generally reserved for the hereditary dysfunction of phosphate regulation which results in large, painless, periarticular calcifications.

So here we have the exact same finding except secondary to chronic renal failure, thus “secondary” or “uremic” tumoral calcinosis. The exact cause is not fully understood by generally believed related to hyperparathyroidism. Interestingly chronic renal failure is actually the most frequent cause of a periarticular calcified mass. And there are no radiographic or histologic differences between the primary or secondary TC.

Findings of TC: 

- Amorphous, sometimes cystic, multilobulated calcifications located about a joint.    

- Can see layering milk of calcium (sedimentation sign). 

- Can be homogeneous (suggesting less metabolic activity and growth)

- Not connected to underlying bone

- No osseous erosion of destruction by the mass

- Typically painless 

- Hip > shoulder > elbow > foot > wrist

Treatment: Primarily dialysis and phosphate depletion (diet, phosphate binders)

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Case 33 Answer

History: abdominal pain. h/o prior abdominal surgery

Answer: Chronic Barium Peritonitis

I think this is a tough one especially without windowing/leveling but what or should I say where is the abnormality?

Lots of high density material right? But hopefully these images show you that this material is NOT within the GI tract.

While Calcium is a possibility, it's all over the abdomen and pelvis and although some may be intranodal or granulomatous, some is clearly intraperitoneal - surrounding the splenic flexure of the colon and linear collections in the upper pelvis

Barium sulfate is (or was <wink>) a commonly used hyperdense oral contrast agent used for intraluminal evaluation of the GI tract

Unfortunately, if leaked into the abdominal cavity it can induce an inflammatory response (even in the absence of leakage of fecal material).

Barium Peritonitis comes in two forms:

Acute - Barium causes a chemical induced inflammation. This can cause large volume exudative ascites actually resulting in severe hypovolemia requiring aggressive fluid resuscitation. This is in addition to any necessary antibiotic therapy for fecal/bacterial contamination.

Chronic - If not removed promptly, barium quickly clumps and adheres to parietal and visceral surfaces and becomes extremely difficult to remove. Fibrosis develops which can yield to repeated bowel obstructions.

Treatment is early laporatomy and extensive peritoneal washout.

Historic mortality rates are as high at 53%. However, despite our improved understanding of the underlying pathophysiology, more recent studies still show mortality rates in the 20-35% range, sometimes higher when there is associated bacterial peritonitis. 

Take home message: It can be easy to see scattered hyperdense material throughout the abdomen and assume it is lymph node calcifications or retained barium within diverticula. I keep this case in mind to remind myself of the possibility and morbidty if it isn’t