DX: Asymmetric Ischiopubic Synchondrosis (van Neck-Odelberg disease)

This is an important variant that we as radiologists have to take in consideration. The ischiopubic synchondrosis (IPS) is the junction between the inferior ischial and pubic rami and is principally composed of hyaline cartilage. Is a temporal joint occurring in childhood prior to fusion of the ischial and pubic bones. With skeletal maturation, like all synchondroses, it becomes thinner and then obliterates, either due to bony union or synostosis.

Here is the spot image:

There is an expansile lesion of the inferior ischial and pubic rami that resembles a lytic bone mass (chondroid matrix). But in this group age, before a bone neoplasm arrises as a differential we have to discard first normal variants or infectious ethiology. Osteomyelitis is a good possibility but there is no history of previous limb or skin infection. Neither there's no history of malnourishment that can induce such infection. 

Therefore, IPS is our main consideration. It can be asymmetric also. But why pain?...if pain presents, we called it Van Neck-Odelberg disease and treat it as a growing pain. Also is good to consider that this disease has correlation with foot dominance.

Here are some examples in literature:

http://www.ijri.org/article.asp?issn=0971-3026%3Byear%3D2011%3Bvolume%3D21%3Bissue%3D2%3Bspage%3D107%3Bepage%3D110%3Baulast%3DMacarini
http://uiortho.com/ioj/2010/08cases.pdf
http://www.virtualpediatrichospital.org/providers/PAP/MSDiseases/IschiopubSynchon.shtml
http://www.ajronline.org/content/182/2/361.full.pdf+html


Thanks for your participation in FB groups.

Until next year!!

CASE 29: 5 y/o male with left hip pain

An infant with chronic left hip pain..Pain was mild and he had no relevant history to our concern.

Differentials?

Later on I'll post the conclusion.

DX: Lumbar spine duplication

Remember the past post?

This case don't needed further description. I pressume that is very clear that there are 2 parallel lumbar vertebraes semideveloped, each one with its own pedicle, vertebral body and laminae.


Patient had a visible, ulcerated open spine defect. CT is great for evaluation of bone structures but we need MRI to clearly define this pathology because it can clearly show the spinal chord and conus medularis, dural sac and meninges. This case was unknown to me, at first I thought maybe it is a severe  form of diastematomyelia (two hemichords?). One thing is a fact, that there is a duplication of almost 3 lumbar vertebraes and latter fusion at sacrum level. This remarcable defect is rare and exceptional.

It i typically associated with severe neurologic abnormalities (dicephalus, myelomeningocele) or gastrointestinal abnormalities (omphalocele, neurenteric fistulas).

The pathologic variants of split cord malformation range from a fibrous septum only partially splitting the cord and acting as a tether point within a single dural sac, at the mild end of the spectrum to gross vertebral anomalies with partial spine duplication and tethering at a fibro-osseous midline mass often associated with a lipomeningomyelocele or neurenteric cyst at the severe end.

For further information please reffer to links below.

Thank you all COBRAns for your participation on FB group.

• http://link.springer.com/content/pdf/10.1007%2FPL00007301
• http://www.ajnr.org/content/25/5/895.full.pdf+html
• http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647508/pdf/i1079-0268-32-1-99.pdf
• http://www.ajnr.org/content/25/5/895.full.pdf
• http://www.experts.scival.com/uic/pubDetail.asp?t=pm&id=9516710&n=Benjamin+A+Goldberg&u_id=767

CASE 28: 3 month old female patient with lumbar neural placode

This is a depictive case..

A newborn ongoing a CT scan due to open lumbar spine defect (Myelomeningocele).

Differentials??..feel free to comment

DX: Chondroblastoma of the hand

Ok sorry for the delay. Here is the reason:

I knew that this patient went to ressection of the hand mass because I found this image:

Later on, I compared with previous hand x-ray prior to biopsy 11 years ago.

We see here an expansile mass with predominantly chondroid matrix. Bening appeareance, but age favors malignancy in bone tumors. So a biopsy was conducted and it revealed : Chondroblastoma

Patient was given a conservative treatment but 10 years later the mass continued to cause pain. This is the radiography control.

Pathological specimen (seen above) revealed: Osteochondroma.

That was the issue. I went to pathologist and the Department decided to conduce a revision of the case. And I was part of the discussion. Imaging findings are clearly narrowing the scope of differentials to a chondroid, benign, slow growing mass with no soft tissue involvement and some diffuse calcifications. STIR and T2 sequences are useful to show the hyperintensity of the lesion due to cartilaginous tissue wich is rich in water content. They reviewed the biopsy with the specimen and concluded that it is a Chondroblastoma.

Either way, this is still a rare lesion in the hand and more rarer in this group age (>50y).

Chondroblastomas most frequently arise in the epiphyses of long bones, with 70% occurring in the humerus (most frequent), femur and tibia 9. ~ 10% are found in the hands and feet wich is this case.

They are seen as well defined lytic lesions, with either smooth or lobulated margins with a thin sclerotic rim, arising in the epiphysis or apophysis of long tubular bone such as the femur, humerus, or tibia. Internal calcifications can be seen in up to 40 - 60% of cases 7,9. A joint effusion is seen in ~1/3 of patients. They range in size from 1 - 10cm, with most being 3 - 4cm at diagnosis.

Approximately 92% of patients presenting with chondroblastoma are younger than 30 years. However, chondroblastomas have been reported to arise in patients as young as 2 years and as old as 83 years. In several large series, most patients were diagnosed in the second decade of life.

Thank you for the patience in this case. Hope is useful.

CASE 27: 64 y/o male with hand bump

Ok here goes this next case.

A 64 year old male with mildly painful progressive swelling in left hand wich was originally suspected to be a cyst, but ultrasound proved it wrong. Unfortunately don't have US images because it was made in another clinic, but the recommendation was to order an MR of the hand. No history of trauma or infection to our concern.

Here are the relevant images:

 STIR CORONAL

 STIR AXIAL

 T1 CORONAL

 T1 POST GAD

 T2 CORONAL

T2 AXIAL

Differentials?

Later I'll post the conclusion of this biopsy proven case.

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DX (presumptive): Cervical Spine Racemous Neurocysticercosis

Hello, after a long time here is my new post. Thank's for all your questions, congratulations and support for this blog. That helps me to stay motivated enough to pursue posting. Ok..a quick reminder of the past case:

Male with quadriparesia..

This was an interesting one. Image findings are consistent with a cervical multicystic mass with extra and intramedullar component. It compresses the cervical cord creating gross edema (mielitis) that is the actual cause of the patients symptoms. Edema ranges from C2  towards C7 level.

The imaging challenge was that the tumor has extra and intramedullar component. Differential diagnosis include Neurocysticercosis, Neurofibromatosis, Schwanomma, Cystic Astrocytoma.

The patient underwent surgery and we were invited to perform an Ultrasound.

  Dr. Leal (neurosurgeon) with a posterior cervical approach. 

That's me (on the right) with Dr. Sanchez (gazing the camera..hehe) prior to surgical ultrasound.

Long axis view of the spine depicting fibrous inflamatory changes. No clear cyst was found.

Anterior border spine echogenicity consistent with fibrous changes.

The spine was engorged and it was no possible for the neurosurgeon to extract any mass without nerve damage. The Dura was very adhesive to spine. 

The patient was given Cysticidal drugs only because of image findings and in matter of weeks miraculosly symptoms have substantially improved. MR control (not posted) showed reduced edema and no extradural mass (only intramedullar). The prognosis is still poor though. The reason is due to the fact that a spinal infarct is highly probable.

http://www.neurology.org/content/77/23/e138.full

http://www.neurology-asia.org/articles/20072_127.pdf

http://www.uscspine.com/conditions/neck-spine-tumors.cfm

Update..

Hello. I'm currently on my Observership of Vascular Interventional Radiology in the renowned Central Military Hospital in Mexico City so I am not posting any new cases till I'm done. Hopefully next month I'll be able to include some of the cases seen here but it's quite difficult due to my training. Even though is not a Fellowship I get to be in most procedures so it's not really an observer work. For that I'm happy :) I will also post the conclusion of the past case. You can comment if you wish.

Here is a pic of the Hospital..

CASE 26: 32 y/o male with progressive cuadriparesia

Patient started several months ago with right hand paresia and subsequently developed to ipsilateral leg and now in all 4 limbs, more present in right side.

He underwent a Cervical MR, here are the relevant slices (click to enlarge):

Differentials please..

Interamerican College of Radiology Congress!

I want to have a time to invite you all foreigners and locals to this years CIR congress wich will be taken place  in El Salvador.

Here is the ad and the webpage for more information:




http://cir2012elsalvador.com/

DX: Vascular Dementia possible Amiloid Angiopathy with État criblé VR spaces

Sorry for the long delay..some very big situations in my life came asn with that all of my time...anyways..

Patient is in worse condition now, MR study was conducted several months ago. Findings are inconclussive but representative of a leukoencephalopathy (white matter disease). The combination of brain atrophy, isquemic lesions (pons and cerebellum) and puntiform (petechial) hemorrage are consistent with a degenerative vascular disease. Differentials are broad but Vascular Dementia and Amyloid Angiopathy are much more likely due to age and symptoms. CADASIL is more encountered in a young population.

White matter disease manifested as hyperintensities on FLAIR and T2 WI:

État crible Virchow-Robin Spaces:

http://radiopaedia.org/articles/peri-vascular-space


Cerebral amyloid angiopathy (CAA), also known as congophilic angiopathy, is a form of angiopathy in which amyloid deposits form in the walls of the blood vessels of the central nervous system.  CAA has been identified as occurring either sporadically (generally in elderly populations).

Amyloid deposition predisposes these blood vessels to failure, increasing the risk of a hemorrhagic stroke. Since this can be caused by the same amyloid protein that is associated with Alzheimer's dementia such brain hemorrhages are more common in people who suffer from Alzheimer's, however they can also occur in those who have no history of  dementia. The hemorrhage within the brain is usually confined to a particular lobe and this is slightly different compared to brain hemorrhages which occur as a consequence of high blood pressure (hypertension)  - a more common cause of a hemorrhagic stroke.

The diagnosis of vascular dementia can be straight-forward in patients with a clear history of strokes and cognitive impairment when a temporal connection exists between stroke and cognitive decline. More often, however, it is difficult to determine whether cerebrovascular disease alone causes dementia, whether it merely contributes to the dementia, or whether it is simply a coincidental finding. Various diagnostic criteria exist to aid diagnosis.

On the Hachinski ischaemic scale vascular dementia is diagnosed when the patient is given a score of 7 or higher. Although the Hachinski scale is widely used, particularly for research purposes, it has poor interrater reliability, and modified versions have been proposed.


http://www.bmj.com/content/312/7025/227.full 

http://emedicine.medscape.com/article/1135408-overview 

http://en.wikipedia.org/wiki/Multi-infarct_dementia 

http://radiopaedia.org/articles/peri-vascular-space 

Thanks for your comments on FB COBRA group!

CASE 25: 77 y/o female patient with altered mental status

Patient with previous semi-vegetative state (alertness only), had sudden loss of consciousness and apparently partial complex seizures. She had progressive deterioration of her mental status and locomotion during a 2 year period.

An MR study was recommended. Here are the relevant images:

DWI were negative for restricted diffusion.

Diferentials please...

DX: Superior Mesenteric Artery (Wilkie's) Syndrome

Wilkie's syndrome has some peculiarity becasue of its rareness and also because of the important role of the radiologist to identify it for proper and rapid surgical approach.

Here are the findings:

CT revealed gas within a duodenal loop wich is also dilated but apparently there is no intra or extraluminal compression. We have to consider that in a normal setting, there is no gas in duodenum.Upper GI series confirmed the obstruction in the 3rd segment (horizontal) and dilation of the 2nd segment (vertical) of the duodenum. CT also showed a narrowing between abdominal aorta and superior mesenteric artery right in the passage of the duodenum consistent with Wilkie's. She underwent suergery that confirmed the duodenal impingement.

Superior mesenteric artery (SMA) syndrome is a very rare, life-threatening gastrovascular disorder characterized by a compression of the third portion of the duodenum by the abdominal aorta (AA) and the overlying superior mesenteric artery. The syndrome is typically caused by an angle of 6°-25° between the AA and the SMA, in comparison to the normal range of 38°-56°, due to a lack of retroperitoneal and visceral fat. In addition, the aortomesenteric distance is 2-8 millimeters, as opposed to the typical 10-20.

 It is also known as Wilkie's syndrome, cast syndrome, mesenteric root syndrome, chronic duodenal ileus and intermittent arterio-mesenteric occlusion.It is distinct from Nutcracker syndrome, which is the entrapment of the left renal vein between the AA and the SMA.

Until next time!..

http://en.wikipedia.org/wiki/Superior_mesenteric_artery_syndrome
http://emedicine.medscape.com/article/932220-overview#a0104

CASE 24: 24 y/o female patient with acute abdominal pain

This case was provided from the renowned Centro Medico Hospital in Guatemala City.

Here is the brief history. Patient had some chronic digestive problems and developed malnutrition and low body weight consequently. She could not eat an entire meal or solids. Parents thought it was an anorexic problem. One day ago she suffered from an acute abdominal pain in epigastrium associated with nausea and vomiting so they decided to bring her to the ED.

She underwent a CT scan. Here is the CT spot image:

With this finding, they suggested an upper GI series (shown below):

Findings and diagnosis?

DX: Xanthogranulomatous Cholecystitis

This was a biopsy proven case that wasn't on my first diagnosis arsenal as a differential.

US gave me the impression  that a bile stone was "impacted" in gallbladder.

CT findings were: focal gallbladder wall thickening with pseudo-impingement at fundus, with no adjacent stones only near the neck. It had IV contrast enhancement. No liver lesions.

Imaging characteristics were not as conclussive as wanted but there was a neoplasic component for sure. I reccomended to correlate with tumor markers especially Carbohydrate Antigen 19-9 (CA 19-9). Results were abnormal so, Gallbladder Carcinoma was the clinical-radiological diagnosis.

She went to surgery and a Cholecytectomy was performed. Biopsy of the specimen was reported as Xanthogranulomatous Cholecystitis (XGC).

XGC is a rare inflammatory disease of the gallbladder characterized by a focal or diffuse destructive inflammatory process, with accumulation of lipid laden macrophages, fibrous tissue, and acute and chronic inflammatory cells. In 1970, it was known by the descriptive term fibroxanthogranulomatous cholecystitis, but in 1981 the name xanthogranulomatous cholecystitis was proposed in a review of 40 cases from the Armed Forces Institute of Pathology. Its importance lies in the fact that it is a benign condition that may be confused with carcinoma of the gallbladder, which is associated with a poor prognosis.

XGC was initially described as a variant of chronic cholecystitis. However, while the latter is usually regarded as a benign condition with questionable clinical significance, xanthogranulomatous cholecystitis is an active and destructive process that can lead to significant morbidity as the inflammatory process usually extends into the gallbladder wall and adjacent structures. Thus, it should be considered a distinct clinical entity.

The pathogenesis of XGC is thought to be related to extravasation of bile into the gallbladder wall from rupture of Rokitansky-Aschoff sinuses or by mucosal ulceration. This event incites an inflammatory reaction in the interstitial tissue, whereby fibroblasts and macrophages phagocytose the biliary lipids in bile, such as cholesterol and phospholipids leading to the formation of xanthoma cells.

Gallstones may have an important role in the pathogenesis, since they appear to be present in all patients. It has been suggested that xanthogranulomatous cholecystitis is analogous to xanthogranulomatous pyelonephritis, which results from obstruction and stasis due to renal calculi.

 A few recent reports have shown a possible association of this disease with carcinoma of the gallbladder.
The inflammatory process often extends into neighboring organs, such as the liver, omentum, duodenum, and colon. The clinical importance of XGC lies in the fact that it can be confused radiologically with a gallbladder carcinoma.

Several reports demonstrated the radiological features of XGC. However, as some are nonspecific, it is often difficult to distinguish XGC from gallbladder carcinoma by the conventional imaging techniques of  ultrasonography, CT and MRI. Moreover, the fact that XGC can infrequently be associated with gallbladder carcinoma makes the differentiation more difficult.

http://www.uptodate.com/contents/xanthogranulomatous-cholecystitis
http://www.ajronline.org/content/148/4/727.long
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721248/pdf/WJG-15-3691.pdf
http://www.surgpath4u.com/caseviewer.php?case_no=660&view=yes&h=&w=&fs=



Hope it was helpful as it was to me..until next time...

CASE 23: 55 y/o female with RUC pain

Patient came to the ED with history of acute abdominal pain, suspected (+) Murphy's sign and mild jaundice. She had previous ultrasound showing gallstones several months ago. Calculous Cholecystitis was suspected so an ultrasound was conduced.

Bloodwork showed an obstructive pattern on billirubin serum levels but also high in Lactate Dehydrogenase and  mild elevation of Alanine Transaminase and Aspartate Transaminase levels. This was a concern to me on hepatic parenquimal integrity.

Here are the US gallbladder (VB) images: (soory the poor quality but click to enlarge)

The suitable exam to better characterize findings is a CT:

I wanted to see first a non contrast phase due to some suspected areas shown in ultrasound that produced posterior acoustic shadowing.

I wanted also a late phase (120 segs) to see the demeanor of the lesion.

Findings?..Differentials?..


Soon the conclusion..