Hepatocellular Adenomas

Hepatic / Hepatocellular adenomas are uncommon benign tumor commonly seen in young to middle aged women, with history of oral contraceptive use. 

👉 Hepatic adenomatosis:  >10 adenomas. Adenomas in hepatic adenomatosis is not related to the hormonal or other risk factors. They tend to be multiple, progressive, symptomatic, more likely to lead to hepatic dysfunction and possible malignant transformation. 

HCAs are now classified based on the genetic and pathologic subtypes as :

1. Inflammatory hepatocellular adenoma.
2. Hepatocyte-nuclear-factor-1-alpha (HNF-1α-mutated) hepatocellular adenoma. 
3. β-catenin-mutated hepatocellular adenomas.
4. Unclassified subtype (includes HCAs without any genetic abnormalities).

Typical hepatic adenomas show moderate arterial phase enhancement with washout in portal venous and delayed, appears isointense to rest of liver. Chemical shift imaging can produce loss of signal of the adenoma in out of phase images due to the presence of fat within.


Name two hepatocyte specific contrast agents?

1. Gd-BOPTA / Gadobenate Dimeglumine
2. Gadoxetate Sodium.

What will happen in case of HCA with hepatocyte specific contrast agents?
Ans : Will appear darker than rest of liver, as the hepatocytes in HCA are non-functional.

Easy to remember Hepatic Adenoma better as ‘Hepatocyte’ Adenoma, as it lacks biliary epithelium, portal vein and even Kupffer cells.

Incidence Ratio in Female to Male is 9:1, Why 

Ans: OCP use. (Anabolic steroids also increase the risk, common with young men).

Surgery is recommended irrespective of size, why?

1. Risk of rupture and shock.
2. Transformation into HCC.

Below MRI images are of a 25yr old female patient who presented with pain related to cholecystolithiasis. Three incidental slightly echogenic lesions are seen in both lobes during USG, for which MRI was suggested.

T2 weighted images showing slightly T2 hyperintense lesion in the superior subcapular portion of the left lobe, lateral segment. 

Another similar signal intensity lesion in right lobe, segment VII/VIII

The main lesion showing the signal intensity loss in the Out-phase images, suggesting intralesional microscopic fat content. No restricted diffusion were seen in these lesions. 

Subtlest of three in the superior portion of segment VII of right lobe, again showing the loss of signal intensity. 

Increasing the TE of T2 WI reduces the signal intensity of the lesion in addition to that of rest of the structures. (c.f. hemangioma shows similar signal on increasing TE). See this article to see how a hemangioma looks like on increasing TE ('The Light Bulb Sign')

  Dynamic post contrast images shows prompt arterial phase enhancement of the lesion (yellow arrow), and appearing someehat isointense to rest of liver in the further images.

References:

1. Luigi Grazioli, Lucio Olivetti, Giancarlo Mazza, Maria Pia Bondioni, "MR Imaging of Hepatocellular Adenomas and Differential Diagnosis Dilemma", International Journal of 
   Hepatology, vol. 2013, Article ID 374170, 20 pages, 2013.
2. Hepatocellular Adenomas: Correlation of MR Imaging Findings with Pathologic Subtype Classification, Radiology.
3. Hepatic Adenomas: Imaging and Pathologic Findings. Luigi Grazioli, Michael P. Federle, Giuseppe Brancatelli, Tomoaki Ichikawa, Lucio Olivetti, Arye Blachar, Radiographics.

Persistent Trigeminal Artery (PTA), Tau sign

Persistent Primitive Trigeminal Artery is one of the persistent carotid-vertebro-basilar anastomoses. PTA arises from petrous-cavernous junction, runs posterolaterally along the trigeminal nerve, crosses over or through dorsum sella.  

Two types of PTA have been described. 

Saltzman Type I : PTA supplies the distal basilar artery. PComs are usually absent. The distal basilar artery is absent or hypoplastic. Distal vertebral arteries are also hypoplastic. 

Saltzman Type II : PTA supplies the Superior Cerebellar Arteries, with PCAs supplied by the PCom. 

TOF MRA images showed Saltzman type I PPTA, where the PTA is seen replacing the distal basilar artery. 

Sagittal MIP MRA image showing the distal basilar artery completely supplied by the PTA. 

The Tau sign, resembling a 'T' is classically described in the sagittal images. 

Eosinophilic Gastroenteritis

Case: 40Y Male patient presented with abdominal pain and diarrhoea. 

Plain CT image shows thickened appearing colon (orange arrows) with surrounding fat stranding. Thickening of anterior pararenal fascia is also seen bilaterally (blue arrows). 

Contrast CT images showed edematous thickening of the terminal ileum (not shown) and large bowel upto distal descending colon. Peri-colonic inflammatory fat stranding is noted. The SMA-SMV, IMA-IMV showed normal contrast opacification. 

Contrast CT images showing mild right pleural effusion (yellow arrow) and ascites (green arrows). 

Differential Leukocyte count revealed Eosinophil count of 18% initially and rose upto 68% within 3 days. Peripheral smear showed normocytic normochromic picture with marked eosinophilia. 

Colonic biopsy showed dense chronic inflammation with predominance of eosinophils - features compatible with Eosinophilic enterocolitis.

Patient was treated with Steroids and Azathioprine, improved and was asymptomatic with normalized lab parameters in the last visit.  

Eosinophilic gastroenteritis  is a rare inflammatory disorder of the gastrointestinal tract, characterized by focal or diffuse eosinophilic infiltration of the gastrointestinal tract. Clinical features and radiological findings are non-specific, so a high index of suspicion is needed, in cases of peripheral eosinophilia (seen in >60%). This usually presents with dyspepsia and diarrhoea. It may rarely cause GOO / SBO and pancreatitis. This disease was first described by Kaijser in 1937.

Although any age group can be affected, majority of patients are in the 3rd to 5th decades, with a slight male preponderance. Most patients have history of seasonal allergies, asthma, food sensitivity, eczema, elevated IgE levels. 

EG is a self-limiting disorder in most cases and usually responds well to steroids. 

Three types of EG have been mentioned, 

1. Mucosal EG (most common) : presents with fecal blood loss, anemia, weight loss due to malabsorption or protein losing enteropathy.
2. Muscularis EG : presents with obstruction (GOO/SBO).
3. Subserosal EG : manifests as eosinophilic ascites. 

Definitive diagnosis of EG requires bowel biopsy correlation demonstrating the eosinophil infiltration. In cases of the subserosal EG, high eosinophil count in a sterile ascitic fluid by paracentesis can also be demonstrated. 

Major DD would be a intestinal parasites, which necessitates stool examination to look for ova and parasites. 

Hypereosinophilic syndrome (HES) is an idiopathic condition associated with marked peripheral eosinophilia (>1500/uL for >6months) and gastroenteritis. Heart, lungs, brain and kidneys are also affected in HES. 

Imaging features are non-specific, can show edematous wall thickening. Ascites and pleural effusion can be seen. Esophagus, stomach, small bowel and also colon can be affected. 

References:

• A Review of Eosinophilic Gastroenteritis.
• Radiopaedia. 

Thanks to Dr. GP. 

Radiation enteritis

Below are the CT images of a 60y female patient, post surgery, post chemo-radiotherapy for Ca Rectum 3 months before the CT. 

CT images show 'long segment, contiguous, mild circumferential wall thickening of distal and terminal ileum, measuring length of ~30cm and maximum wall thickness of ~6mm. No peri-enteric fat stranding or lymph node enlargement seen'.  There were no sinuses or fistulae or any features of bowel stricture or obstruction.  

The blue arrows point to the thickened ileal loops. 

Radiation induced enteritis, especially of the small bowel is less often seen even though small bowel is very radiosensitive, because of its relatively increased mobility. Among small bowel the terminal ileum is the most sensitive, as it is more or less fixed. Fixation due to adhesions from a previous surgery or previous inflammation (including PID) can increase the risk of radiation induced bowel damage. Thin habitus, diabetes and hypertension can also influence the post radiation injury. 

Radiation doses >50Gy administered over 6 weeks can produce radiation induced bowel injury, which in 10% of cases might require surgical intervention. ~5-15% patients receiving >45Gy develop chronic radiation enteropathy.

The three stages of radiation enteritis are acute, subacute (2-12 months) and late phase. Acute phase is usually the mucosal inflammation, crypt abscesses, superficial ulcerations. Subacute phase, is a phase of regeneration, arteriolar sclerosis. Late phase is usually due to fibrosis. This phase can result in strictures, obstruction, fistula and sinus formation. 

👉  Point to remember : Keep in mind the differential of radiation induced bowel injury, in cases of bowel wall thickening. Especially in a post op patient, ask for history of radiotherapy. 

Perineural cysts (Tarlov cysts) of the cervical spine

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).