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..