Calyceal Diverticulum

Calyceal diverticula are outpouchings of renal calyces or even renal pelvis (pelvi-calyceal diverticula) into the renal cortex connected by narrow neck. These are lined by non-secreting urothelium (transitional cell epithelium).

Incidence: 0.2-0.6% of patients undergoing renal imaging.

Usually these are incidental findings and are mostly asymptomatic. Due to stagnation of urine within the diverticulum, these are prone for stone formation. Stones can be found in upto 50% of the calyceal diverticula.

Exact etiology of the formation of calyceal diverticula are not known, may be congenital or acquired due to infections, VUR, or rupture of a cortical cyst.

These are subdivided into two types:¹
Type 1 communicating with a calyx, usually found in upper pole.
Type 2 communicating with renal pelvis, larger, usually found in mid-pole (also called pyelo-calyceal diverticula). Radiopaedia adopts a slightly varied types, with type 1 from minor calyx and type 2 from major calyx or renal pelvis.²

There may be internal calcifications, either in the form of stones or of milk of calcium. In one small ultrasound series, 7 of 11 cases of calyceal diverticula demonstrated mobile echogenic material. It is suggested that the presence of mobile hyperechogenic material within a cystic structure is diagnostic of a calyceal diverticulum. ³

Differential considerations of a calyceal diverticulum would include complex cyst, dilated calyx, cystic renal neoplasm and abscess. Unless an excretory (or urogram) phase is acquired diagnosis of calyceal diverticulum is not possible. Dilated calyx can be due to obstructing stone, tumor or due to infundibular stenosis in TB.



The following plain and contrast CT images are of a 40 year old male patient who was evaluated for left lumbar pain and tenderness.

Plain CT Axial sections showing calcific focus within a subtle hypodense area in the bilateral renal parenchyma. 

Type I Bosniak cyst is noted medially (not marked).

The above three images shows the Plain CT, venous phase and excretory phase axial sections of both kidneys, which shows contrast filling of the cystic appearing area in the venous phase - consistent with the diagnosis of Calyceal Diverticulum of both kidneys. Calculus formation is noted in both these calyceal diverticulum. 

Oblique coronal MIP image showing the contrast filled bilateral calyceal diverticulum (Green arrows). The yellow arrow points to the pathology for which the patient underwent the CT examination (colitis). As in most cases, this case of bilateral calyceal diverticulum was also asymptomatic.  

3D VRT image demonstrating the calyceal diverticula. 

References
1. Mullett, Rebecca et al. “Calyceal diverticulum - a mimic of different pathologies on multiple imaging modalities.” Journal of radiology case reports vol. 6,9 (2012): 10-7. doi:10.3941/jrcr.v6i9.1123

2. Stunell, H et al. “The imaging appearances of calyceal diverticula complicated by uroliathasis.” The British journal of radiology vol. 83,994 (2010): 888-94. doi:10.1259/bjr/22591022

3. Reynard J, Brewster S, Biers S. Oxford Handbook of Urology. Oxford: Oxford University Press; 2006. p. 328.

4. Leveillee RJ, Bird VG. Treatment of Caliceal Diverticula and Infundibular Stenosis. In: Smith AD, Badlani G, Bagley D, et al., editors. Smith’s Textbook of Endourology. 2nd ed. Ontario: BC Decker; 2007. pp. 171–185.

Incisive Canal Cyst (Nasopalatine Duct Cyst, NPDC)

Incisive canal cyst also known as nasopalatine duct cysts (NPDC), is a developmental cyst arising from the epithelial remnants of nasopalatine duct, a duct connecting the nasal cavity with anterior maxilla in fetal life. It is considered the most common non-odontogenic cyst of jaw bone.

Often it presents in 4th to 6th decades, with slight male predilection. Patients may be asymptomatic, or can have pain, discharge and swelling often due to infection.

Incisive canal cyst is often >15mm in size, whereas the normal finding of incisive foramen is not expected to cross 6mm in diameter.  These cyst is seen superior to the roots of the maxillary incisors and usually doesn't result in any root resorption, but can sometimes result in displacement of the incisor roots.


Below are MRI images of incidentally detected Incisive canal cyst in a 50 year old male patient. MRI was done for evaluation of headache. T2 weighted sagittal, coronal and axial images shows a hyperintense cystic lesion in the anterior maxilla with mild displacement of the roots of maxillary incisors. Cyst measured 13.3mm in width.

Cyst was isointense to muscle in T1 WI (not shown), and hyperintense in T2 FLAIR images (not shown).

See another case of Incisive Canal Cyst : CT images HERE.

Superficial Temporal Artery Pseudoaneurysm

Pseudoaneurysms of the superficial temporal artery are an uncommon vascular lesion of the external carotid system and most often the result of blunt head trauma. Causes include sports-related trauma, non-sports related trauma, i.e. gun-shot wounds, assault, etc., and iatrogenic causes such as after cyst removal, punch hair grafting, and craniotomies.

The anterior branch of the STA is most vulnerable to injury from blunt trauma due to its superficial course and close proximity to the underlying bony structures.

The time period from craniotomy to pseudoaneurysm in the literature varied between 4 days and 3 months. Differential diagnoses for STA pseudoaneurysm include vascular tumor, arteriovenous fistula, meningeal artery aneurysm with bony erosion, subcutaneous lipoma, abscess, and localized hematoma.

The following is a case of left Superficial Temporal Artery pseudoaneurysm in a 69yr old female, arising after a trauma to the side of the head, hitting an open window, 2 years back, with transient loss of consciousness. Swelling was slowly increasing in size.

The ultrasound image below shows a clear defect in the STA vessel wall of ~6.8mm length, with the pseudoaneurysm measuring ~16mm x 11mm.

References:

Superficial Temporal Artery Pseudoaneurysm: A Case Report

Syed Muneeb Younus, Muhammad Imran, Rabia Qazi

Front Surg. 2015; 2: 51. Published online 2015 Oct 6. doi: 10.3389/fsurg.2015.00051

PMCID: PMC4593946

Primary repair of a traumatic superficial temporal artery pseudoaneurysm: case report and literature review. Ayling O, Martin A, Roche-Nagle G, Vasc Endovascular Surg. 2014 May; 48(4):346-8.

Ruptured pseudoaneurysm of the superficial temporal artery after craniotomy.

Honda M, Anda T, Ishihara T, Neurol India. 2013 Nov-Dec; 61(6):698-9.

http://www.ajnr.org/content/cow/10252010

Septic arthritis of hip joint

 Young male patient with fever of ~5-6 weeks duration, right hip pain.

STIR Coronal : Green arrow - joint effusion, Orange arrow: asymmetric red marrow / marrow edema.
(See last MRI image also)

STIR Axial image, Grade 3 joint effusion

STIR Axial image, marked.

Thickening and enhancement of the joint capsule / synovial layers.

Ultrasound: Echogenic fluid with debris within the anterior synovial recess. Anterior peri-articular muscle edema+. Probe tenderness+.

Eventhough the T1 hypointense signals in the intertrochanteric region (left) can be explained by the presence of residual red marrow in this 20yr old patient, the signal intensity is markedly reduced on right side, suspicious of marrow edema.

UR- Quiz 1 - (4th June 2018) : What's your diagnosis?

 69y Female. History of  transient loss of consciousness and fall resulting in side of head hitting a window, 2 years back, with slowly progressing swelling in left side of head.

ANSWER HERE...

Ring shaped lateral meniscus

Ring shaped lateral meniscus is a very rare anatomical variant which can easily mimic and make it difficult to distinguish from a bucket handle tear. Unlike the normal C-shape, this variant forms a complete ring.

Usually the lateral portion appears as in normal cases, with angular margins or sometimes can appear deficient anteriorly. The additional medial component appear like displaced torn fragment and easily gets mistaken for a bucket handle tear (where the body of meniscus will be truncated c.f. ring meniscus).

In differentiation from central perforation of a discoid lateral meniscus, the inner margins in central perforation will be irregular with degenerative changes. Associated osteophytes and chondral lesions may also be seen unlike a case of ring shaped lateral meniscus.

Pancreatic pseudocyst with duct communication (CT)

Pancreatic pseudocysts are the most common (85% to 90%) cystic lesions of pancreas, which are encapsulated peripancreatic or remote fluid collections developing after 4 weeks of an episode of acute pancreatitis. These are called pseudocysts as cyst lining is formed of fibrous tissue and not true epithelium. Cyst contents are rich in amylase.

Causes of pancreatic pseudocysts include Acute or chronic pancreatitis (most common), pancreatic trauma and rarely iatrogenic (e.g. partial gastrectomy). In cases of acute pancreatitis with inflammatory changes and seeing fluid collection developing wall or capsule in the peri-pancreatic region in follow-up imaging, is usually diagnostic of a pseudocyst. These usually arise 4 to 6 weeks after an acute episode. Pseudocysts can be followed up if the patient is asymptomatic or the cyst is smaller than 6cm as there is a chance of spontaneous resolution in smaller cysts.¹

Complications include secondary infection, hemorrhage, rupture and mass effect on adjacent structures.¹

Above axial images of contrast CT shows a large, peripherally enhancing cystic area (green arrow) in relation to the pancreas, consistent with a pseudocyst. Yellow arrow points to the pancreatic head head and orange arrow points to the distal CBD.

 

Green arrows mark the pancreatic pseuocyst and blue arrow points to the stretched residual pancreatic parenchyma of body region.


 

Sagittal reformats showing the duct (yellow arrows) in tail region.

Sagittal MPR and Sagittal Minimum Intensity Projection, showing the PD and the pseudocyst.

A communication between the PD and the pseudocyst is demonstated in the above image. 

Cysts communicating with PD are difficult to treat and tend to recur.

Presence of internal dependent debris level is regarded as highly specific for the diagnosis of pancreatic pseudocysts in MRI ².




References:
1. Imaging Diagnosis of Cystic Pancreatic Lesions: Pseudocyst versus Nonpseudocyst
Young H. Kim, Sanjay Saini, Dushant Sahani, Peter F. Hahn, Peter R. Mueller, Yong H. Auh
Radiographics, May 2005.

2. Differentiating Pancreatic Cystic Neoplasms from Pancreatic Pseudocysts at MR Imaging: Value of Perceived Internal Debris.
Michael Macari, Myra E. Finn, Genevieve L. Bennett, Kyunghee C. Cho,
Elliot Newman, Cristina H. Hajdu, James S. Babb.
Radiology April 2009.

3. Radiopaedia.

Plain CT Brain findings in an adolescent patient with Tuberous Sclerosis

Tuberous Sclerosis (TS) or Bournville disease is a rare Autosomal Dominant (AD) neurocutaneous syndrome (phakomatoses) characterized by development of multiple benign tumors of in various organs. Since the characteristic clinical triad mentioned is mental retardation, adenoma sebaceum and seizures is uncommon, imaging plays an important role in diagnosis of this condition.Sometimes intrauterine diagnosis of TS of the fetus can be suspected with visualization of cardiac rhabdomyomas in ultrasound.

Below are some of the features of TS detectable in plain CT, in a 16yr old patient.

Above image shows the presence of characteristic calcified and non-calcified sub-ependymal nodules (red arrows). Calcification of these subpendymal hamartomas is less frequent in early childhood, where as cortical/subcortical tubers can calcify as early as 2yrs of age.

Image showing multiple cortical and subcortical hypodensities suggestive of cortical tubers (blue arrows). Most of the tubers in TS are located in frontal lobe.

Left foramen of Monro region shows a relatively homogenous, non-calcified lesion (blue arrows) measuring AP dimension of ~13mm - suspicious of a Subpendymal Giant Cell Astrocytoma (SGCA / SEGA). These are considered WHO-Grade 1 tumors, eventhough there is a potential of causing obstructive hydrocephalus. These are theorized to evolve from the subpendymal nodules. Histologically both SGCA and subpendymal hamartomas show same appearance.SGCAs can show intense enhancement, and may show calcifications and heterogeneity.

Same lesion in sagittal reformat (golden arrow).

A few calcified cerebellar tubers (green arrows).

Above bone window images show multiple calvarial
small sclerotic areas of hyperostosis (orange arrows).

Acute Cholecystitis with intrahepatic perforation of GB causing secondary liver abscess

Above image shows distended gall bladder with pericholecystic fat stranding (orange arrow) consistent with acute cholecystitis.

Above post contrast CECT portal venous phase images showed focal small defect (yellow arrow) in the GB wall suggesting GB perforation, with abscess formation in segment V of right lobe. Blue arrow points to a single calculus within the GB lumen.

Serial axial sections showing small air pocket (orange arrow) within the liver, with adjacent heterogenous hypodense areas (yellow arrow),  superior to the hepatic abscess in segment V. If looked carefully complete pancreatic atrophy, with smooth duct dilatation and intraductal calculi can also be seen, consistent with Chronic Calcific Pancreatitis.

Eventhough acute cholecystitis is a common entity, GB perforation is rare and rarer still is its intrahepatic perforation. GB perforation is commoner in males. Risk of perforation is more in acalculous cholecystitis due to sepsis and associated co-morbidities.

Obstruction of cystic duct causes increased intraluminal pressure which inturn results in impared lymphatic and venous drainage. This results in vascular impairement leading to wall necrosis and finally perforation.

Niemeier classfied GB perforations into 3 types,
Type 1: Acute : Perforation with generalized biliary peritonitis.
Type 2: Subacute : Perforation with pericholecystic abscess and localized peritonitis.
Type 3: Chronic : Perforation with cholecysto-enteric fistula (Original classification did not include intrahepatic perforation / internal fistulae).

Treatment is with antibiotics and percutaneous drainage initially, followed by interval cholecystectomy. Open drainage and cholecystectomy has also been performed.



References:

Date RS, Thrumurthy SG, Whiteside S et al. Gallbladder perforation: case series and systematic review. Int J Surg 2012; : 63–68

Bilateral basal ganglia T1 hyperintensity

Left image shows normal T1 signal intensity of Globus Pallidus, where as
right T1 axial image in a 54yr old male with known chronic liver disease
 shows bilateral globus pallidus T1 hyperintensity.

 

Right image: Another CLD patient with bilateral T1 hyperintensity of Globus Pallidus.

Common causes of bilateral T1 hyperintense basal ganglia include:
1. Physiologic calcification.
2. NF-1
3. Hepatic Encephalopathy.
4. Hyperalimentation (Patients undergoing parenteral feeding).

Less common causes:
1.HIE (Term HIE, Hypoxic cerebral infarction).
2. CO poisoning.
3. Kernicterus.
4. Wilson's Disease.

Rarely thyroid / parathyroid hormonal imbalances, hypoglycemia, Fahr's disease, Hallervorden-Spatz syndrome, JE, Congenital HIV etc. also may cause T1 hyperintensity of the basal ganglia.

In chronic liver disease / cirrhotic patients there is symmetrical T1 hyperintensity in Globus Pallidus and Substantia Nigra.


References:
1. Expert-DDx Brain.

Hibernomas

A hibernoma is a rare benign fatty tumor arising from the vestiges (remnant / trace) of fetal brown fat. It is predominantly seen in 20-40 yrs age group with a slight female predilection. It is named so because of resemblance to brown fat in hibernating animals.

Most often the lesion is located in subcutaneous regions of the back (periscapular /interscapular region), neck, axilla, shoulder, thorax, thigh and retroperitoneum. Rarely these are also seen in scalp, breast, peri-ureteric region and scrotum.

Hibernoma usually manifest as slowly growing painless soft-tissue mass. Sometimes patient can be symptomatic due to compression of adjacent neuro-vascular structures, for example sciatica in a posterior thigh lesion.

In ultrasound these usually appear as hyperechoic lesions. Angiography will reveal lesional vascularity with arterio-venous shunting. These can mislead due to increased uptake in 18-FDG-PET.

In CT these lesions show low attenuating lesion, slightly higher attenuating than the subcutaneous fat. Enhancing septae may be seen, with lesion showing mild enhancement. MRI usually demonstrate lesion to be isointense to subcutaneous fat in most cases, with intervening enhancing sepatations. Reduced T1 and T2 signal intensity is also described in few cases. Contrast enhancement need not be present in all cases.

Additionally prominent lesional vessels may be seen in the ultrasound or as T2 flow voids in MRI, with can cause torrential hemorrhage during biopsy, especially in deep seated lesions.

Case courtesy of Dr Matt A. Morgan, Radiopaedia.org. From the case rID: 37589

Above image shows an intermuscular lesion between the gluteus medius and maximus muscles, with intermediate attenuation between fat and muscle. Prominent feeding vessel is seen along the lateral margin of the lesion.

Pre-operatively differentiating from liposarcomas is difficult. Four histological subtypes have been defined: Typical (~80%), Myxoid (8%), Lipoma-like and spindle cell variant. 'Typical' variant has predominantly brown fat. Myxoid variant is seen more often in men with higher water content (increased T2 signal). Lipoma-like lesion is seen more commonly in thigh, more resembling adult fat.


References:
Imaging Findings of a Hibernoma of the Neck
A.C.B.S. da Motta, D.E. Tunkel, W.H. Westra and D.M. Yousem
American Journal of Neuroradiology September 2006, 27 (8) 1658-1659;

CT and MR characteristics of hibernoma: six cases
Dursun, Memduh et al.
Clinical Imaging , Volume 32 , Issue 1 , 42 - 47

From the Archives of the AFIP
Benign Musculoskeletal Lipomatous Lesions
Mark D. Murphey, John F. Carroll, Donald J. Flemming, Thomas L. Pope, Francis H. Gannon, and Mark J. Kransdorf. RadioGraphics 2004 24:5, 1433-1466

Transient Synovitis of Hip Joint

Transient Synovitis (Coxitis fugax) is the most common cause of acute hip pain in children aged 3 to 10 years. It is a self-limiting acute inflammatory condition which is managed symptomatically. However it needs to be differentiated from Septic Arthritis, which will require antibiotics and surgical drainage.¹

Over 90% of hip joint effusions can be attributed to transient synovitis. ²
It has a male gender predilection and more frequently affects the right hip joint.

Etiology of transient synovitis remains unknown. Various theories include response to infection (URTIs), trauma, allergen / antigen etc. Clinical, laboratory and radiological findings help in differentiating Transient Synovitis from Septic Arthritis. The latter is usually associated with fever, elevated ESR & CRP.

X-Ray may reveal mild joint space widening due to effusion. Ultrasound is often the initial modality as it can reliably assess presence of joint effusion in the anterior recess.

MRI findings of Transient Synovitis include:
1. Joint effusion.
2. Synovial thickening & enhancement.
3. Adjacent soft tissue edema, with characteristic absent bone marrow edema.
4. Contralateral effusion (lesser volume usually).

Below MR images are of a 10yr old girl child with limping showing features of transient synovitis in right hip joint. No bone marrow edema or contra-lateral effusion is seen in this child. Grade 3 joint effusion is present in right hip joint.

Very rarely Transient Synovitis can cause osteonecrosis. But most often with analgesics and other symptomatic treatment, it resolves gradually, without any known long term sequelae. Eventhough it is most commonly seen in children, tranisent synovitis can also develop in adults.

Hip joint effusion is graded according to Mitchell Classification. 0 : None, 1 Minimal, 2 - Enough to surround the femoral neck and 3 distension of joint recesses.

References:

1. MR imaging of transient synovitis: Differentiation from septic arthritis. Pediatric Radiology, 2006.
2. Radiopedia.

Bilateral symmetrical enlargement of Lacrimal Glands

Causes of bilateral symmetrical enlargement of lacrimal glands include:

1. Sarcoidosis. (Usually associated with systemic sarcoidosis. Rare to have isolated lacrimal gland involement).
2. Lymphoma.
3. Leukemia.
 
Lymphomatous involvement of lacrimal glands usually shows restricted diffusion in MRI.

4. Sjogren Syndrome (autoimmune condition affecting salivary and lacrimal glands, F:M ratio of 9:1, seen in 4th and 5th decades of life, Early stages glands can become enlarged, to atophy in the later stages).


Less common causes of symmetrical lacrimal gland enlargement include:

5.  Mikulicz syndrome - Previously considered as a subtype of Sjogren, now being considered as a part of IgG4 related disease spectrum.

6. Kimura disease - usually presents as painless enlargement of neck lymph nodes and salivary glands, with associated blood eosinophilia, raised serum IgE, associated soft tissue masses. Affects males of 20-40yrs in 80% of cases.

7. Primary Lacrimal Amyloidosis.


Lacrimal glands measures ~4-5mm usually. A visual / subjective assessment is usually sufficient for making the diagnosis of enlargement.




References:
1. Lacrimal Glands: Size Does Matter!, Middle East Afr J Ophthalmol. 2011 Oct-Dec; 18(4): 328–330.
2. Radiopaedia.

ACL avulsion fracture

ACL avulsion fracture is the fracture of the tibial attachment of ACL at the anterior intercondylar region.

Zaricznyj modification of Meyers and McKeevers classification is the most used system, which divides these fractures into 4 types, with type 3 further divided into 3a and 3b.

Type 1 : Minimally / Non-displaced fragment.

Type 2 : Anterior elevation of the fragment.

Type 3 : Complete separation of the fragment.
   
         3a - Involves small portion of the eminence.
         3b - Majority of eminence is involved.

Type 4 : Comminuted avulsion or rotation of the fragment.

T1 WI showing Type 4 (Comminuted) Avulsion fracture in a 21yr male.

Type 3b ACL Avulsion fracture in an 18y female patient.

Aortic Dissection : Stanford Type B

Patients with abdominal pain often undergoes CT evaluation for further assessment after a baseline USG. Diagnosing aortic dissection is easy in post contrast CT (Angiogram) images, but when the patient comes for CT Abdomen, reasonable observation and high degree of suspicion is needed, to proceed with CT Chest and Abdomen Angiogram (rather than abdomen alone), otherwise we would end up taking multiphase images of abdomen alone. The therapeutic decision in dissection depend upon the detecting the involvement of preductal aorta (Stanford A), which requires emergency surgical management. Thus if we fail to detect / suspect dissection in plain study, we have to take repeat angiogram of the thoracic aorta later.

The following is a case of a 40yr old female patient who presented with abdominal pain radiating to back. USG did show slightly prominent aorta for age, which is actually a good pickup, since there was no other abnormality in abdomen.

CT Abdomen was requested for further evaluation of the abdominal pain. In the plain CT sections, the aorta was seen dilated, with proximal abdominal aorta measuring up to ~3.5cm in outer diameter. Highest section of the scan did show the dilated distal descending thoracic aorta with hyperdense peripheral crescent, indicating acute intramural hematoma (/thrombosed false lumen of dissection), which necessitates the scan to be taken from arch vessels to iliac arteries, to assess the involvement of ascending aorta, arch and to look for the inferior extent.

Dilated proximal abdominal aorta, raising the suspicion of dissection in a 40yr old female patient.

Hyperdense crescent indicating acute intramural hematoma.

Above image shows the proximal end of the intramural hematoma, beginning just distal to the left subclavian artery origin, making it a Stanford type B dissection. Ascending aorta and arch branches were not affected (not shown).

The hyperdense hematoma can be seen slightly rotating / whirling in an anticlockwise fashion, to come towards the left lateral aspect of aorta (see below), from the posteromedial aspect.

The dissection flap was only visualized from the D11 vertebral level.

The above image showing relationship of the true lumen (green arrow) and false lumen (orange arrow). As going distally the false lumen is seen enlarging in size.

3D-VRT images showing the dissection flap (yellow arrows).


It's important to determine the origins of branch vessels before endograft or stent placement to avoid end organ ischemia.

Axial sections showing the origins of major abdominal aortic branches, with true lumen on right and false lumen on left side. Celiac trunk, left renal artery and IMA are seen arising from the false lumen.


Dissection is the spontaneous longitudinal separation of intimal and adventitial layers because of blood traversing and splitting through the media. The inciting factor is due to an intimal tear, which allows the blood to enter into the media. The additional lumen thus formed within the media is called as the false lumen.

Aortic dissection is divided into two types according to the Stanford classification. If ascending aorta is involved then its termed type A and if it involves aorta distal to the left subclavian artery alone then its termed type B dissection.

The high attenuation within the aortic wall is either due to acute intramural hematoma or due to hyperdense false lumen.

Sometimes within the hyperdense false lumen, residual flow can be seen (as shown below).

Residual flow channel in false lumen (Orange arrow).

References:
1. AJR 2001 July article.
2. RG March-April 2010 article.