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141 Cards in this Set

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Renal mass
Is there a significant cystic component, or is it predominantly solid?
Predominantly solid
Is there macroscopic fat (i.e. NOT just suppressing on out of phase imaging)
yes, there is macroscopic fat
AML

2 Things to do:


1) Measure it -- if larger than 4CM, needs to be embolized to prevent hemorrhage


2) Look for other evidence or stigmata for TS, especially if patient is young and has multiple bilateral AMLs
No, there is no macroscopic fat
RCCA until proven otherwise


Imaging findings (i.e. infiltrating bean or renal coll system tumor suggesting TCCA) or clinical history (i.e. young male with sickle cell suggesting Renal medullary CA) may suggest another diagnosis, BUT REGARDLESS there is no way to exclude malignancy, and they all come out.
Significant cystic component
Bosniak classification


Group them mentally into BENIGN and SUSPICIOUS categories.
Benign features
= B1 and B2 classifications


NO FURTHER EVALUATION REQUIRED
Bosniak 1
TOTALLY SIMPLE CYST

-imperceptible or very thin wall

-no Ca

-no septations

-no nothing
Bosniak 2
- Thin septation (may have PERCEIVED enhancement, since thin enhancement in these really cant be determined definitively)

- Fine calcified rim or septation
Bosniak III
Thick or irregular or enhancing wall or septation


Chunky calcification
What then is IIf?
Characteristics between a pure II and a definite III. Instead of ripping it out, follow-up imaging is preferred since only a small proportion of these (maybe 10-20%) will turn out to be malignant
Bosniak IIf
NO MEASURABLY OR DEFINITELY ENHANCING COMPONENTS


3 characteristics:


1) Minimal SMOOTH thickening of wall or septations


2) Increased # of thin septations


3) Hyperdense cysts larger than 3CM
What is Bosniak IV
Cystic RCCAs. These are actually primarily solid tumors which have a cystic component, unlike the others which are truly cystic lesions.

What differentiates these from the IIIs is that the soft tissue mass is more extensive, not just related to the cyst.
Staging of RCCA
I

II

III a b c

IV a b
Stage I RCCA
Confined to renal capsule
Stage II RCCA
Penetrates renal capsule, but confined to Gerota's fascia.


Can involve ipsilateral adrenal gland.
Stage IIIa RCCA
Renal vein involvement (may extend into IVC)
Stage IIIb
Local nodal involvement
Stage IIIc
Both vascular and local nodal involvement
Stage IVa
Distant nodal involvement

Invasion of adjacent organs
Stage IVb
Distant mets
RCCA with mass in ipsilateral renal vein
Must determine whether this is extension of tumor or just bland thrombus due to hypercoagulability

Decide with doppler ultrasound or enhanced MRI with subtraction.

Difference is potentially very significant both in regards to treatment and prognosis.
Cystic RCCA
PAPILLARY RCCA
RCCA with mass in ipsilateral renal vein
Must determine whether this is extension of tumor or just bland thrombus due to hypercoagulability

Decide with doppler ultrasound or enhanced MRI with subtraction.

Difference is potentially very significant both in regards to treatment and prognosis.
DDx for solid renal mass
ANY patient:


RCCA


TCCA


Lymphoma


Mets


Patients with specific history

Sickle cell -- Renal medullary CA

VHL -- MULTIPLE RCCAs
Cystic RCCA
PAPILLARY RCCA
DDx for solid renal mass
ANY patient:


RCCA


TCCA


Lymphoma


Mets


Patients with specific history

Sickle cell -- Renal medullary CA

VHL -- MULTIPLE RCCAs
RCCA with mass in ipsilateral renal vein
Must determine whether this is extension of tumor or just bland thrombus due to hypercoagulability

Decide with doppler ultrasound or enhanced MRI with subtraction.

Difference is potentially very significant both in regards to treatment and prognosis.
Cystic RCCA
PAPILLARY RCCA
DDx for solid renal mass
ANY patient:


RCCA


TCCA


Lymphoma


Mets


Patients with specific history

Sickle cell -- Renal medullary CA

VHL -- MULTIPLE RCCAs
DDx multiple bilateral renal masses
1) METS


2) Lymphoma/Leukemia -- NON-Hodgkins


3) Multiple RCCAs (VHL)


4) TB
Patterns of renal lymphoma
4


Perinephric encasement from retroperitoneum -- VERY SPECIFIC but uncommon appearance


Multiple bilateral masses


Diffuse enlargement


SINGLE RENAL MASS -- mimics RCCA
Solitary renal mass and small hypodense lesion of spleen
Think LYMPHOMA
Clue that its lymphoma
Since exceedingly rare to have primary renal lymphoma, will have other evidence of lymphoma elsewhere

--RP lymph nodes
--Hilar enlargement
--Neck nodes enlarged
etc
Hypodense renal mass.
Ask for HU
HU is 15
ASK FOR THIN SECTION IMAGING TO CONFIRM THE PRESENCE OF MACROSCOPIC FAT

Caveat -- large soft tissue mass with tiny dot of fat can RARELY be RCCA engulfing renal sinus or perinephric fat. But that is very uncommon.
TS transmission
AD but up to 50% new mutations
Prognosis of TS
POOR

75% mortality by age 20!
% patients with AML who have TS
20%
% patients with TS who have AML
80%


So, its 80/20 in the obvious direction
Only time solid renal mass does not come out
1) Patient has history of lymphoma and single renal mass -- this is one of two cases that you would biopsy to see if RCCA or lymphoma, because lymphoma treated with chemo


2) Can do same thing if patient has a primary malignancy, or may just take it out assuming its a RCCA. If it is RCCA, that is actually better for the patient as its better to have two different malignancies in remission than one same malignancy that is metastatic. Whether biopsied or not, something HAS to be done in order to get the information needed.
Renal mass and surrounding perinephric soft tissue density
2 Possibilities

Give contrast to determine whether surrounding soft tissue density is FLUID or SOLID


If fluid, it is high density fluid, probably blood. Mass is probably AML. DO FAT SAT TO CONFIRM MACROSCOPIC FAT. RISK OF PAGE KIDNEY.


If peripheral lesion is enhancing and solid, likely retroperitoneal lymphoma with renal invasion
Angiogram with AML
May not see entire mass as blush. WHAT YOU SEE ARE THE FOCAL ANEURYSMS WITHIN THE AML.
Treatment of bleeding AML
COIL THE ANEURYSMS
Patients at increased risk for RCCA
Prior history of RCCA


VHL


Renal cystic disease of dialysis
What is not associated with increased risk of RCCA
Autosomal dominant PCKD; but it is harder to diagnose by imaging
Most common adrenal masses
Nonfunctional adenoma


METS


That is why we are always trying to differentiate between these two
Adrenal cysts common or uncommon
RARE, just like thymic cysts
Macroscopic fat in adrenal
Myelolipoma. No DDx
What can myelolipomas be associated with?
congenital adrenal hyperplasia
HU for adenoma
under 10
Evaluation of adrenal mass in patient with known malignancy
1) Noncontrast CT shows adrenal mass with HU 10 or lower. Enhances post contrast (rules out cyst) -- Evaluation complete, lesion is adenoma
Mass is greater than 10 HU on precontrast CT
DDx at this point is

1) Lipid poor adenoma


2) Metastasis


MRI is not useful for evaluation of lipid poor adenomas, since they tend not to suppress on out of phase images.

Thus, the next step in evaluation is the contrast enhanced CT with washout imaging.


The reason this works is that ADENOMAS HAVE RAPID WASHOUT


Only 2 values are required at this point: The precontrast doesn't matter anymore. It was above 10, so we don't care about it. All we care about now is how the lesion is washing out, so all we need is:

Post-contrast (portal phase)

15 minute delay
What next
The portal phase image is considered the peak, and we calculate what percent WASHOUT occurs at 15 minutes. We are interested in the percentage DROP in HU during this interval.


portal - delay / portal


So, if precon was 42, postcon 150, and 15 min delay 45, then you calculate the percent washout as:


150 - 45 / 150 = 105/150 = 0.7

or think of it as total amount of washout (in HU) / original HU


Simple calculation
What next
If percent washout is 0.6 or GREATER, it is a lipid poor adenoma.
What if percent washout is 0.52?
Can consider going to MRI
What is criteria for adenoma on MRI?
20% or greater loss in signal between in and out of phase sequences
Why does chemical shift occur?
Not all protons are the same. Like we learned in organic chemistry, a proton spins at a rate largely dependent on the ambient magnetic environment, but also slightly dependent on its own LOCAL environment. For water, the proton sitting there attached to a single oxygen molecule with just one other proton attached to it has a different home environment than the proton attached to a carbon of a hydrocarbon (lipid), which itself is then attached to other protons and at least one other carbon attached to more protons.


These differences in home environment make for very small differences in spin frequency. The difference in spin frequency is dependent on the overall spin frequency (which is much faster) which is itself dependent on the ambient field strength.


At 1.5 T, the spin frequency difference occurs at such a rate that the two spins are exactly in phase every 4.4 ms. That means that halfway between these intervals, the spins are exactly out of phase.

So, you have your RF pulse, and that sets all the spins exactly in phase. Then you set your TE to 4.4 milliseconds, and get images with fat and water in phase.

Then you do the RF pulse again, but this time you set your TE to 2.2 milliseconds. Now fat and water will be exactly out of phase. Thus, if there are 1000 water protons and 1000 fat protons in the same voxel, (and nothing else) there will be signal void. The proportion of signal dropout in each voxel is related to closeness in number of fat protons to number of water protons.
T1WI
Short TR

Short TE
T2WI
Long TR

Long TE
PDWI
Long TR

Short TE
Practically, how do you decide if its an adenoma or not on MRI?
Look at adrenal on in-phase image, and compare its intensity to EITHER SPLEEN OR SKELETAL MUSCLE. You use these as a reference because they have NO FAT in them, and will not change on opposed phase images. DO NOT use liver, because it frequently is fatty infiltrated.


Then look at the out of phase images, and check to see if there is signal dropout RELATIVE TO SPLEEN OR SKELETAL MUSCLE versus its appearance on the in phase images.
Size of adenomas
Should be LESS THAN 4 CM
An adrenal lesion is still indeterminate after all this mumbo jumbo
CT GUIDED BIOPSY

(just think of Hochsztein going nuts when you are unsure if adrenals are one of the things that should not be percutaneously biopsied because of tract seeding) -- That is for ovarian neoplasms mainly.


BUT YOU MUST MAKE SURE THE LESION IS NOT A PHEO BEFORE YOU AGREE TO DO THE PROCEDURE. CHECK BP, LABS, HISTORY. BIOPSYING A PHEO IS BAAAAD
CT guided adrenal biopsy
MAKE SURE IT IS NOT A PHEO FIRST!!!

YOU WILL GET FRIED ON THE BOARDS IF YOU DON'T EXCLUDE PHEO FIRST
Adrenal adenoma on T2 WI
Usually Dark
Adrenal mass bright on T2WI
CLASSIC APPEARANCE OF PHEO


Howerver, most pheos are not light bulb bright on T2, just mildly bright.

Another characteristic is LATE ENHANCEMENT, just the opposite of an adenoma. -- Why late enhancement? They tend to have few feeding vessels and a large extracellular space, so it takes a long time for the contrast to diffuse in.
PHEOCHROMOCYTOMA
10% RULE


10% BILATERAL

10% MALIGNANT

10% EXTRAADRENAL
Adrenal mass, when should you think of pheo
ANY ADRENAL MASS IN PATIENT WITH HYPERTENSION. Of course the HTN may be unrelated, but you MUST RULE IT OUT.
Big mass adjacent to kidney
ADRENAL CARCINOMA, especially if there is associated central necrosis or hemorrhage
How big are adrenal carcinomas usually
90% are over 6 cm, so if you see a 3 cm adrenal mass, its probably not and adrenal CA, and definitely not in Louisville
What do adrenal CAs commonly do?
Invade IVC


Invade spleen and kidneys


Mets to liver
DDx for solid adrenal mass that is not an adenoma or a myelolipoma
Met


HEMORRHAGE (pseudocyst)


Pheo


Adrenocortical CA


Lymphoma
What would hemorrhagic adrenal pseudocyst probably look like on boards?
Bright on T1, so you ask for fat suppressed image. Doesn't suppress. You ask for in/out of phase. Doesn't fall out. So its not fat making the signal high on T1, what else could it be? Proteinaceous cyst? Melanoma met? Probably not. MUCH MORE LIKELY HEMORRHAGE.
Renal pathology, not a tumor
There are 3 things to evaluate:


Morphology/position of the kidneys
--look for congenital (pelvic) or acquired (cysts) abnormalities




Ureters and renal vasculature

--Look for disease but also look for anatomical variants

Parenchyma

--Striated nephrogram
--Prolonged nephrogram
etc
DDx when empty renal fossa
Ectopic kidney (pelvic, crossed fused) -- Look for the normally inserting ureter in crossed fused


Renal agenesis or MCDK that totally regressed
Complication of all ectopic kidneys
ALL prone to reflux


ALL prone to stone formation
Complications of horseshoe kidney
Increased risk for traumatic injury
Horseshoe kidney
Increased risk for Wilms


Increased risk for UPJ obstruction


Associated with VATER


Associated with Turner's
Congenital renal lesion
ASK TO SEE UTERUS TO DIAGNOSE ASSOCIATED MULLERIAN DUCT ABN
Bicornuate uterus
ASK TO SEE KIDNEYS TO DIAGNOSE ASSOCIATED RENAL ABNL
Unilateral large kidney
Infiltrating tumor


OBSTRUCTION


RVT


PYELO


CYSTIC RENAL DISEASE


Contralateral absence of kidney


Klippel-Trenaunay
Klippel-Trenaunay
Hemangiomas and hemihypertophy


So one kidney is bigger. On that same side, proliferation of fat and muscular enlargement
Bilateral renal enlargement
Cystic renal disease


Deposition diseases like amyloid


Leukemia (less commonly lymphoma for this appearance)


Lupus -- think of Charlie's wife


HIV NEPHROPATHY


SINUS LIPOMATOSIS -- The parenchyma is not enlarged, but the kidney is because of fatty proliferation in the renal sinus


Edema
HIV nephropathy
Rapid onset of elevated creatinine progressing to renal failure


2 phases

In the acute phase, both kidneys become edematous, so large and hypodense on CT (non-con, since in renal failure)


Then they shrivel down to atrophic kidneys in the chronic phase.
Kidney expansion of renal sinus with fat
Renal sinus lipomatosis
Renal sinus lipomatosis
Proliferation of renal sinus fatty tissues due to chronic irritation


History of chronic infections, chronic hydronephrosis, persistent renal calculi.


Can result in renal parenchymal atrophy in late stages, and can cause pain due to capsular expansion necessitating nephrectomy for palliation.
Simple renal cysts
Can be symptomatic when large, and can rupture from trauma.
DDx multiple renal cysts
Autosomal dominant -- Larger cysts. Some hyperdense due to hemorrhage. How frequently should you follow them for development of RCCA? -- NOT AT ALL. NO INCREASED RISK.


Autosomal recessive -- in older children/adults who have less aggressive forms and survive, see more organized appearance of smaller cysts than you do in ADPCKD. Also see splenomegaly. All have some degree of hepatic insufficiency.


Acquired renal cystic disease -- LOOKS JUST LIKE Autosomal dominant PCKD. BUT if patient is on dialysis, and did not have cystic disease PRIOR to being put on dialysis, then this is the answer.
Autosomal dominant PCKD
MUST SCREEN THEM FOR BERRY ANEURYSMS
Lots of cysts, patient on dialysis
DID PATIENT HAVE CYSTIC DISEASE BEFORE DIALYSIS??? (i.e. is ADPCKD the cause of the renal failure)

No? Then its acquired renal cystic disease of dialysis.


INCREASED RISK FOR RCCA
Acquired renal cystic disease treatment
1) Screening for RCCA if short life expectancy


2) Bilateral nephrectomy -- not done as frequently anymore

Now . . .


3) Put in transplant kidney -- risk returns to near baseline
Renal cyst with focal calcification at the dependent aspect
FLIP THE PATIENT OVER AND RE-SCAN


If the calcification moves, the patient does not have a cyst. The patient probably has a calyceal diverticulum.


CONFIRM BY GIVING CONTRAST and looking on delayed images for contrast eventually entering the diverticulum.
Calyceal diverticulum
Sequela of prior infection or papillary necrosis


STONE FACTORY due to stasis
Lots of calcifications contained in a structure on plain film
IN RUQ -- Gallstones


IN LUQ -- THINK CALYCEAL DIVERTICULUM WITH LOTS OF STONES
IVP with calyces pointing down
DDX = DUPLICATED COLLECTING SYSTEM (drooping lily) vs. HYPERMOBILE KIDNEY (renal ptosis)
Differentiate renal ptosis from duplicated collecting system
In duplicated collecting system, the lower pole moitey is compressed inferiorly by the dilated obstructed upper pole moiety. But since the kidney is split into 2 moieties, the lower pole moiety will have fewer calyces than a normal kidney will.

Hypermobile kidney is just a normal kidney that is not as well attached as a normal one.


YOU CAN NOT USE DILATION OF THE CALYCES AS EVIDENCE FOR REFLUX INTO A LOWER POLE MOIETY OF A DUPLICATED COLLECTING SYSTEM BECAUSE THE HYPERMOBILE PTOTIC KIDNEY GETS UPJ OBSTRUCTION DUE TO KINKING, IN FACT THAT IS WHY THEY PRESENT IN THE FIRST PLACE
How many calyces is normal?
12 - 14

So count em; if too few its duplicated collecting system
VCUG performed, and demonstrates reflux into a BLIND ENDING URETER
Most commonly due to MCDK which has regressed

Also ectopic insertion of ureter, with subsequent hydronephrosis and eventual regression of that kidney, or you may just be seeing the obstructed moiety's ureter, and the other one is not refluxing.


Prior nephrectomy (for RCCA or trauma, NOT for TCC because the entire ureter is resected in those cases due to likelihood of occult neoplasm in the remaining ureter).


And finally, what you are seeing may just be a ureteral diverticulum, and not the real ureter leading to the kidney.
Given CT or US of kidney through midpole and no sinus fat
FACELESS KIDNEY


If normal anatomy otherwise -- duplicated collecting system


If medullary pyramids disorganized, think MASS
Dilated calyces
LOOK AT RENAL PELVIS


If renal pelvis is distended, its probably obstruction or reflux.


If renal pelvis is not distended, think congenital megacalyces (megacalicosis).

To confirm its megacalicosis, all you have to do is COUNT THE CALYCES. There are TOO MANY with congenital megacalyces.
Congenital megacalyces (megacalicosis)
Associated with 3 things:



Congenital megaureter


Ureterocele


Contralateral UPJ obstruction
Dilated ureter
May be CONGENITAL MEGAURETER


Associated with prune belly? Check in peds section
UPJ obstruction causes
Usually idiopathic, due to muscular dysfunction in ureter


Crossing vessel -- accessory renal artery.


Mass


Circumcaval ureter


Retroperitoneal fibrosis
UPJ obs treatment
Urologist goes in with a scope, and uses a balloon with a cutting edge to incise the UPJ (endopyelotomy), almost like a myotomy for pyloric stenosis, but from the inside

BUT IF THE CAUSE IS A CROSSING VESSEL, THE PROCEDURE WILL NOT WORK AND THE PATIENT MAY BLEED HEAVILY AND/OR LOSE PART OF THE KIDNEY


Therefore, secondary causes of UPJ obstruction must be sought in all cases, to include MRA or CTA to exclude such pathology and eliminate incidence of such catastrophes.
When suspect crossing vessel
ADULT WITH UPJ obs

50% of them are caused by crossing vessel, versus only 10% in peds
IVP or urogram or VCUG with proximal right ureter coursing medial to lateral margin of vertebral bodies.
Circumcaval ureter


DDx: could be due to retroperitoneal fibrosis or mass. USE CT or CTA or MRA to confirm.
Lots of filling defects in upper urinary tract
1) Must always consider multifocal TCC


2) If history of infection: Pyelouretritis cystica


3) Malakoplakia -- Malka (benign)


4) Leukoplakia -- PREMALIGNANT. More common in bladder.


5) Chronic renal vein thrombosis -- with formation of lots of collateral veins causing little vascular impressions
Most important prognostic factor in bladder CA
Depth of invasion
Advanced TCC?
Invade deeply into muscularis propria. 50% have occult metd.
Most common GYN malig
endometrial,
ovarian,then cervical
Stage I cervical
confined to cervix
Stage II
IIb or not tIIb
Bilateral adrenal masses
Adenomas


Mets


Hemorrhage


Pheos
Bladder filling defect
Neoplasm

Calculus


Blood clot


Fungus ball


(same for anywhere in collecting system)
DDx for TOA
Ovarian neoplasm, but different presentation
Tx of TOA
ABX. Only drain complex cases that dont resolve
Calcification in scrotum outside of testis
Scrotal pearl
Meaning
Benign. Assd with hydrocele
From?
Torsion of appendix testis
Large intratesticular calc
BURNED OUT SEMINOMA
Cause of striated nephrogram
Pyelo

Ureteral obstruction


Contusion can look like it
WHy in pyelo
interstitial edeme causes urinary stasis in tubules, which do not opacify
Dilated renal pelvis
Could be obstructed, but more commonly due to paralysis by bacteria
Bladder calculus
Is it midline. If off midline, think displacement of stone by mass or enlarged prostate

Bladder tic with stone

ureterocele with stone
Lots of small dots in proximal part of fallopian tube on HSG. = ampullary part
Salpingitis isthmica nodosa (SIN)


Tuberculosis of the fallopian tube


Tubal adenomyosis
Contraind to HSG
Menstrual bleeding


Acute PID


Recent D and C -- 4 days


Pregnancy
DDx hypointense nodule in peripheral zone on T2WI
CA

BPH nodule

Prostatitis


Hemorrhage post biopsy
Normal peripheral zone
HYPERINTENSE ON T@
Mass in a huge bladder
THATS NOT THE BLADDER. THATS PELVIC ASCITES, and the lesion is probably ovarian.
Ovarian malignancy
Size greater than 6 cm


Solid component


Mural nodules


Internal papillary projections


Thickened septations


Lymphadenopathy


ASCITES
Most common adrenal cyst
Endothelial cyst
Next most common
Lymphangioma
Calcified cystic structure
ADRENAL CYSTS COMMONLY CALCIFY
Mural enhancement in what appears to be adrenal cyst
Thats OK. Allowed to enhance, like pseudocyst.
Calcified renal mass
REGADLESS OF PATTERN OF CALCIFICATION, any renal mass with calcification is RCCA until proven otherwise
Complete DDx of bladder mass
CA


Calculus


Blood clot


ureterocele


Less likely: Fungus ball, focal cystitis
Percent bladder tumor TCC
90%
Percent SCC
5%
Rest
2% adeno CA
US image of uterus
LOOK AT ENDOMETRIAL STRIPE THICKNESS, and suggest endometrial CA if it is at all thick
Testicular microlithiasis
Associated with testicular neoplasm, cryptorchidism, testicular atrophy, infertility