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Fetal echogenic bowel

commonly found in 3rd trimester, uncertain clinical significance.
When found in second trimester, can be normal or associated with
particularly 21
intrauterine growth retardation (IUGR),
bleeding, cystic fibrosis (CF),
congenital viral infections
cytomegalovirus (CMV),

Use 5 MHz probe or less. Turn down gain to see only bowel and bone.

1-less echgenic than iliac crest
2-equal to iliac crest
3-more echogenic than crest
Adverse outcomes associated with grade 2 and 3.


Gestation sac can be seen at about 5 weeks.
should be round
about 2mm thick walls.
grow more than 1.2 mm per day.
Should be in mid or upper zone
Low placement or irregular shape implues abnormality
Gestational sac 10mm or more that is empty may represent blighted ovum or pseudosac of ectopic pregnancy.

Yolk sac should be seen at 5-6 weeks

Embryo can be seen by 6 weeks
Embryo over 5 mm without cardiac activity implies demise

Before 5 weeks, can see intradecidual sign or double decidual sign.

Phases of endometrium

Thin stripe with some endometrial or endocervical fluid at or just after menstruation
Thickens toward ovulation.
Periovulatory (late proliferative phase) is the classic 3 stripe appearance. Measures up to 1.1 cm at this time.
Within 48 hours after ovulation loses 3 stripes and becomes hyperechoic throuhgout. Can thicken up to 1.6 cm.

Retained products of conception.

Heterogeneous tissue in uterus. May look like homorrhage.
May or may not have blood flow.
For remaining trophoblastic tissue, peak systolic blood flow of 21 cm/s is cutoff.
Can develop calcifications if left.

Postmenopausal uterus

Becomes smaller, with thin echogenic endometrium
Endometrium should be 5 mm or less, homogeneous. Biopsy anything over 5 mm.
Can thicken with hormonal therapy. If cyclical, image after progestin (thinnest phase) to find pathological thickening.
If unapposed estrogen, 8mm is the cutoff, biopsy anything more.

Two vessel cord

There is only one umbilical artery in the cord, so two vessels are seen, one artery and one vein.

Imaging findings
Transverse section of cord shows two vessels
Doppler at bladder level demostrates only 1 umbilical artery
In 70% it is the left which is absent
The single remaining UA is enlarged to acomodate extra flow
15% associated with IUGR
A hypoplastic UA is within this spectrum (one large, one small)
Associated with other fetal anomalies.

Fused umbilical arteries
Umbilical artery thrombosis
Excessive wharton jelly

When associated with other anomalies, 50% are associated with aneuploidy, trisomy 18 and 13. NOT 21

Overall rate is 1-2% of all pregnancies.

Imaging the gallbladder

An 8 hr fast is ideal, but still ok of not.
Use a 3-5 hz probe
Bladder neck is very important to emage because stones can be missed in this location

Normal bladder is ,4 cm in transverse diameter and <10 cm long. Wall should be 3mm or less and lumen should be anechoic


are found in 10% of US population
75% are cholesterol and 25% pigment
Most are asymtpomatic. 2% per year become symtpomatic. Biliary colic in RUQ is the most common presenting symtpom.

Sono has 95% sensitivity for detection of stones and a near 100% negative predictive value.
Sones under 3mm diameter may not have a shadow, but not dependent of material.

Differential includes polyps (which are not mobile), Sludge balls (mobile but no shadow)

Floating are cholesterol stones on top of sludge


wall-echo-shadow complex occurs when the gallbladder is entirely filled with stones

The first line is fat interfact- hyperechoic
Second line is the muscle layer, hupoechoic
Third is the surface of the stones, hyperechoic


Is made up of calcium bilirubinate granules and cholesterol crystals.
It forms a fluid level
Can coexist with stones
The sludge itself is usually very homogeneous, but can be heterogeneous or layering look
Can cause pancreatitis due to the cholesterol crystals

Signs of early acute cholecystitis

Stones, wall over 3 mm thick, gallbladder is enlarged and pericholecystic fluid. Sono Murphy's sign is positive

Signs of advanced cholecystitis

There is pericholecystic fluid. Sloughed membraned in the gallbladder, irregular or striated wall or with sonolucencies. Wall disruption, wall ulceration, focal wall bulging

Acute cholecystitis

Usually due to obstruction of the cstic duct or gallbladder neck
Surgery indicated within 48-72 hours or can do ABx course first
PPV of stones on exam is 92%. PPV of sono murphy's sign is 95%. Thick gallbladder wall alone is nonspecific
Increased gallbladder width os more indicative of cholecystitis than increase in length.
Pericholecystic fluid is seen in less than 20% of cases-usually wrost ones. Fluild appearance between the gallbladder and liver is more likely edema than actual fluid

US is preferred modality because it can diagnose other causes of RUQ pain if cholecystitis is not the acutal problem and flase positive cases still usually require surgery because there are gallstones present.

Acalculous cholecystitis

Usually only occurs in the very sick, such as after major surgery, severe burns, major trauma or long term TPN. In these patients, just because there are no stones, does not mean there is no cholecystitis.

Gallbladder cancers

Most are associated with gallbladder stones.
More often in women, and prognosis is not good.
80% have local invasion at presentation and liver or portal nodes
Most common appearance is if of soft tissue mass in the gallbladder, usually on the fossa side, and obliterating the lumen.
15-30% present with diffuse wall thickening which is irrgular, asymmetric or eccentric.
Least common is intraluminal polypoid type, which is usually >1 cm

Differential includes tumefactive sludge, inflammatory wall thickening, polyps, mets, focal adenomyomatosis

Gallbladder polyps

If <5 mm, no further evaluation necessary
5-10 mm range, monitor
over 10 mm romove due to malignancy risk

Cholesterolosis - triglycerides, precholesterols and cholesterol esters are deposited in galbladder lamina propria. Not related to serum cholesterol level, atherosclerosis, DM or stones
There are usually no imaging findings. Polyps are formed in only a minority of cases.

Most common polyp is Cholestrol polyp
Usually have papillary fronds filled wtih lipid laden macrophages buzz-word "ball on the wall" sign
These are usually <5 mm and rarly over 1 cm.
There is no shadow. It is non-mobile, distinguishing them from sludge balls

Less common types : adenoma, pappiloma, leiomyoma, lipoma, neuroma. All these neoplastic types are usually large-ish and have internal blood flow.

Mets to gallbladder

Melanoma has most "tendency" to do this, but still infrequent


is a form of hyperplastic cholecystosis (cholesterolosis is the other)
There is mucosal hyperplasia, thick muscle layer and Rockitansky-Aschoff sinuses which represent herniation of mucosa into muscle layer and contain cholesterol crystals with a bright comet tail.

Gallbladder masses

Tumefacttive sludge

Chronic cholecystitis

Causes of gallbladder wall thickening

AIDS cholangiopathy
Sclerosing cholangitis
Wall infection
Cystic duct obstruction

Non-biliary, which is usually concentric:
Hepatitis causes marked thickening
Heart failure
Lymph obstruction

Porcelain Gallbladder

is extensive wall calcification
associated with chronic inflammation
in 95% cases there are also gallstones
There is 13-60% increased cancer risk, therefore prephylactic ectomy recommended
May present only as partial anterior wall arc of calcification because it starts focally and then spreads

Differential includes WES complex and emphysematous cholecystitis

Liver arteries

Common hepatic arises from celiac axis, then passes anterior to portal axis until the gastroduodenal branch
Proper hepatic starts at that point, ascends in the gastroduodenal ligament to porta hepatis to birfurcation to right and left.
The right hepatic passes posterior to the CBD and anterior to the portal vein

Hepatic artery variants

Replaced right hepatic artery arises from SMA in 20% of population, passes properly through porta hepatis
Replaced left hepatic artery arises from the left gastric in 20% of population, then passes through fissure for ligamentum venosum instead of through porta hepatis

Hepatic simple cyst

Most common focal lesion of the liver. As all cysts, anechoic with posterior enhancement

Complex cystic liver lesions

Cystic mets
Hemorrhagic or necrotic tumor

Rarities include biliary cystaedomas

Vascular lesions are easiliy identified with doppler

Hepatic hemangioma

Most common benign liver neoplasm, occurs in 7% of population, women more. Also most common focal lesions after simple cyst
10% are multifocal
Anusual to be symptomatic
Kassabach-Meritt syndrome when very very large

On US, homogeneous hyperechoic, usually <3 cm (classic look occurs about 60-70% of the time)
Atypical presentation may include preiphreal hyperechogenicity with central hypoechogenicity (reverse target sign)

Blood flow is mostly too slow to detect with doppler
Usually stable over time. 1015% decrease overtime, and only 2% enlarge
This is the ONLY lesion known to change appearance in the span of the exam

If there are no other ristk factors, no futher eval if necessary

Hyperechoic hepatic masses

Hepatocellular CA
Focal fat infiltration

Focal nodular hyperplasis

2nd most frequent benign hpatic lesion after hemangioma, actually associated with hemangiomas, especially multifocal type
10-20% of FNH are multifocal
Lesion is supplied by the arterial network.
One of the lesions with a spokewheel pattern.
Women make up 80-90% of patients
NOT related to birth control

Sono appearance varies. Most are isoechoic to liver. Possible to have calcific and cystic changes, but necrosis is very uncommon

Doppler is best for imaging the spoke-wheel. Usually the dominant feeder arter comes from outside to the center, and then it brances that radiate back out.

Differential includes fibrolamellar HCC, adenoma, regular HCC, hemangioma, vascular mets

Hepatic adenoma

Rare and benign
Hs a few kupfer cells, but no ductules.
Either has no capsule, or is incomplete
Most common in women on birth control. Risk is related to the risk and duration.
In men, there is risk from use of anabolic steroids
Can be multiple in association with type I glycogen storage disease.

They have propensity to bleed, but there is low risk of malignancy

Simple adenomas are usually hypoechoic
When there is hemorrhage, become heterogeneous with complex cystic structure
10% have calcifications
Free fluid seen in cases of rupture

Mets to liver

Liver is one of the most common sites for mets
LFT is an unrealiable indicator
Most mets are mltifocal and involve both lobes

Most liver mets have a target appearance, iso or hypoechoic center with hypoechoic halo. A thick halo represents a region of proliferating tumor

Hepatic Taget lesions

After mets, the next most common cause of taget lesion is HCC followed by lymphoma, abscess, adenoma and FNH

Calcified hepatic mass

Large CALC with or without mass
Fibrolamellar hepatoma
Old hematoma
Old abscess

Small calc without mass
Biliary stones
Hepatic arteries

Causes of diffuse hepatic enhomogeneilty

Common Uncommon
Cirrhosis HCC
Mets Hepatic fibrosis
Farry infiltration Lymphoma


Most common primary malignancy of the liver
There is strong association with hepatitides and cirrhosis and any other chronic pathology.
Growth patterns are variable, solutary, multifocal, diffuse, infiltrating, large dominant with satellites.
There is a strong predisposition to invade vascular structures 30-60% of cases.
Tumor thrombus expands the lumen more so than bld thrombus and has arterial flow indise detectable on Doppler, which is HEPATOFUGAL

Sensitivity of US is decreased by 50% in severe cirrhosis due to heterogeneity of the parenchyma.

Adenomatous hyperplasia

Nodule that is larger than the rest of the regenerative ones in a cirrhotic liver

Fibrolamellar HCC

An unusual variant of HCC
The typical patient is younger than regular HCC and usually there is no coexistant chronic liver disease
Has a better prognosis alos.

On US, solitary and mor likely calcified than regular HCC

Hepatic lymphoma

Usually seen in the setting of advanced systemic disease. Usually non-Hodgikin type
Primary hepatic lymphoma is usually seen in the setting of immunocompromise (same as brain)

Sono appearance is a target lesion or homogeneous mass

Hepatic bascess

Usuaaly secondary seeding
Classic appearance is a complex fluid collection, b ut may mimick a solid mass (especially initially)
Gas causes high reflection and ring down artifact
May calcify with healing

Differential includes hematoma, hemorrhagic cyst, necrotic/hemorrhagic tumor

Fungal hepatic abscess

Usually secondary to immunocompromise
Most common cause is candida, which usually formas a microabscee, but sometimes can make a very large abscess

Typically has arget appearahce with central hyperechoic region and periphareal hypoechoic halo.
After healing become hymogeneously hyperechoic and may calcify.

Granulomatous hepatic disease

Pneumocystic carnii may be the cause in immunocompromise such as AIDS.
Treatment for the lung disease misses the liver (aerosol)

The characteristic appearance is a multifocal echogenic foci scatter throughout the liver.
Similar appearance may be seen with M avium or CMV

Hydatid hepatic cyst

Range from simple cyst giving rise to mutifocal duaghter cysts. There may be floating debris

Amoebig hepatic cysts

Happens by seeding throught the portal system from a primary colonic infection
Indistinguishable from a puogenic abscess


Rare in the US, but common worldwide
The infection is in periportal tiss, resulting in thick portal triads.


Usually there are no detectable sonographic abnormalities
Sometimes there is increase hyperechogenicity of protal triads-small bright areas in the liver periphery

Fatty hepatic infiltration

In the US, the number 1 cause is obesity, followed byt EtOH
Other causes include cholesterol lowering meds, chemo, corticosteroids, DM, malnutrition, TPN, toxins (carbon tetrachloride)

Can leave focal normal areal than then look like a hypoechoic lesion. The typical location for this are anterior to right portal, at portal bifurcation and around gallbladder at adjacent to the falcine ligament.

Portal flow

provides 75% of blood to the liver, but only 50% of the O2 to the liver.
There s little or no pulsatility.
Normal velocity is 20-30 cm/sec

In portal hypertention, portal vein can be up to 13 mm

Causes of portal hypertention

Intrahepatic Extrahepatic
Portsinusoidal Prehepatic
Cirrhosis Portal thrombus
Veno-occlusive Compression

Presinusoidal Posthepatic
Fibrosis Hep vein thrombus
Lymphoma IVC abstruction
Sarcoid Constrictive

Arterioportal fistula

Look for collaterals-
Umbilical vein drains to inferior episatric
Coronary vein is posterior to the left lobe, normally 6 mm or less
Look foe any reversal of flow in the portal tributaries or in the portal itself "hepatofugal"

Sign sof portal HTN on US

Increased diameter of the portal vein, 13 mm
Increased size of hepatic arteries
Hepatofugal flow

Sensitivity of US is 90%. Flase negatives are very uncommon.
Negative predictive value is 98%

Causes of blunted hepatic vein pulsativity

Collateralization of the hepatic vein
Diffuse metastatic disease
Transplant rejection

Arterioportal fistula

Conjenital or post traumatic (biopsy)
Multilobular cystic mass with arterior flow

Causes reversal of flow in the portal system
Can be seen with Osler-Weber-Rendu usually tiny and not detectable by US

Hepatic conjenital defects

Right heart failure increases pulsatility in hepatic veins "W" shaped waver secondary to increased antegra and retrograde components
Tricuspid regurgitations inverts the systolic anegrade flow resulting in only 1 antegrate pulse from diastoly

Hepatic transplant complications

Arterial lesions are words, biliary ducts have only arterial supply.
Suspect arterial obstruction when there is no doppler flow.
Resistive index <0.4 is always arterial obstruction
0.4-0.5 should raise suspicion
Reversed arterial flow is due to collateralization which is due to thrombosis or stenosis

Portosystemic shunt

When normal there is flow in the shole lumen and portal flow is reversed into the stent
Normal velocity range is 90-190 cm/sec

Signs of stenosis
Elevated velocities (aliasing on doppler)
elevated maximum and depressed minimum volocities
Low poral vein velocity
Change of volocities between exams
Reversed flow in the draining hepatic vein into the shunt
Portal flow away from the shunt

Porta hepatis anatomy

The transverse view of the porta hepatis is mickey mouse, where the head is the portal, left ear is the artery and right ear is the bile duct

The right hepatic artery passes between the CBD and portal vein in 85-90% of population, most of the rest have variant artery anterior to the CBD.

Biliary obstruction

Normal hepatic ducts are no more than 40% as wide as the adjacent vein and no more than 2 mm peripherally

Criteria for biliary obstruction
Diameter >2 mm peripherally or over 40% the diameter of the adhacent vein
Increased throughtransmission
Irregular tortuous walls
Stellate configuration centrally
No doppler signal.
Extrahepatic mid/segment diameter (between R hepatic and pancreas) over 7 mm

Fatty meal evaluation- normally the sphincter would relax, let the bile out and diameter of ducts would decrease. With obstruction the sphincter relaxes but bila can't come out, plus there is stimulus to produce more bile, leading to increased diameter of the ducts overall


US can detect all stone types since all have increased signal. Shadowing seen in about 80%
Most are seen distally in the ducts, near the ampulla
Moar are pigment stones from deconjugation in the ducts.
Often multiple
Easily onfused with bilary gas. With gas there is often ringdown artifact. Stones don't ring.

Predisposing factors
Bile stasis
Bacterial infection (enteric)
Recurrent pyogenic cholangitis
Flukes lead to bacterial infection leading to stones


Most common location is at the bifurcation of the common hepatic duct - otherwise known as a klatsin's tumor
5% are multicentric
Most common pattern is infiltration of the duct wall producing stricture.
Less common pattern is intraluminal polypoid or diffuse sclerosing.

Sono appearance - abruptly terminating dilated duct. poorly marginated and isoechoic to liver.

Differential varies by location
In distal duct - pancreatic or ampula carcinoma, mets
At duct confluence - GB carcinoma, HCC

Nonresectability - when there are hepatic mets, invasion of portal vein, encasement of hepatic artery

Biliary duct wall thickening

A nonspecific sign. Can be smooth or nodular
One importan cause is sclerosing cholangitis
Over 5 mm thickening with disproportionate dilation of intrahepatic ducts is very suspicious for choangiocarcinoma

Cystic biliary duct diseases

All types much more prevalent in women
Result from anomalous connection to pancreatic duct possibly

I - fusiform outpuching of extrahepatic ducts
II - diverticular outpouching
III - choledochocele = dilation of distal intramural portion of CBD, which protrudes into the duodenum
IV - multifocal extra and intrahepatic cysts
V - is Caroli's disease

Classic triad of symtoms is Jaundice (80%), palpable mass (50%) and abdominal pain (50%)

Differential includes duodenum, cystic duct remnant, mesentery or omentum, pancreatic pseudcyst, right kidney, liver cyst or hepatic artery aneurysm

Caroli's disease

Multifocal saccular dilation of INTRAHEPATIC ducts.
There are many complications including stones due to stasis, obstruction, cholangitis, liver abscess.
Associated with hepatic fibrosis, cystic disease of the kidney (medullary sponge particularly)

Dominant feature of this thing may be kidney failure (go figure)

Mirizzi syndrome

CBD obstruction from outside by a calculus impacted in the cystic duct or gallbladder neck

Kidney sono anatamy

Central fat in the sinus is hyperechoic
There are usually 11 pyramids in adults but only 9 calyces meaning that some are doubled.
Cortex is equal or hypoechoic to liver, which is hypoechoic to spleen.
Upper limits of longitudinal length is 13 cm, lower limit is 9 cn.
Ectopic kidney or agenesis results in empty fossa and an enlarged ipsilateral adrenal taking up the space.

Vascular variants include retroaortic or circumaortic renal veins (mostly left) which is seen in 3-17% of population.

Hydronephrosis stages

I - mild to slight distention of the calices (elsewhere says no blunting)
II - medium distention readily evident dilation (with blunting) without thinning of the cortex
III - severe dilation with thinning of the cortex

Causes of hydronephrosis

Common Uncommon
Obstruction Active diuresis
Previous obstruction Diabetes Insipidus
External pelvis Reflux
Distended bladder

More on hydronephrosis, obstructive

True obstruction can lead to an arterial resistive index over 0.7 or asymmetry of resistive index greater than 0.1
Look for urinary jets in the bladder - with obstruction they can be absent or low level continuous instead of high level periodic.
Sensitivity of US in detection is 95%

Flase negative can be due to partial dehydration or only mild obstruction
False positives due to dilated renal cessel, peripelvic cyst, chronic reflux, nephropathy, severe papillary necrosis

Renal cysts differential

Caliceal diverticuli
Pappilary necrosis
Obstructed upper pole

Peripelvic cyst

Likely lymphatic ductule in origin
No communication to collection system or vasculature
Ofetn bilateral and multiple


Multiple variable size cysts in kidneys
Most are bilaterally, eventually replace most of the kidney.
50% cases incolve the liver too.
Most important thing to differentiate is the kidney size, PCKS enlarges the kidneys
Mass effect can obstruct the collecting system
Increased risk of calculi form stasis.
Crystals in cysts produce ringdown artifacts.
Many cysts are hemorrhagic producing complex appearance. This is MUCH more common than neoplasm, so watch a complex lesion, no need to go after it right away.

NO associated risk of cancer

Criteria for diagnosis
- 2 cysts (ipsilateral or 1 cyst each kidney) in a person under 30 with a 1st order affected relative
- 2 cysts or more in each kidney in a person from 30-59
- 60 years or more, 4 or more cysts are required each side.
PCKD is unlikely if no cysts are seen by age 30.

Acqured kidney cystic disease

With time occurs in most dialysis patients (90% at 3 yars)
Commonly enlarges the kdiney like PCKD
Hemorrhage is common
7% risk of solid neoplast, most are <3 cm
risk is 3-6x of the general population

von Hippel-Landau in kidneys

Most common overall associated neoplasm is RCC (25-50%, and upt o 75% when there is acutal renal involvement)
Retinal angioma is seen in 60% and CNS hemangioblastoma in somewhere over 50%.
30-70% of patients have kidney involvement with multiple renal cysts.
Generally the kidneys are not enlarged (compare to PCKS or acqured polycystic disease)
Cyst wall thickening is suspicious of malignancy - watch carefully


makes up 90% of primary renal masses, making it the most common solid renal mass in adults. Assume any solid mass in adult is RCC till proven otherwise.
There is a cystic type, but it makes up only 5% overall. Has thick septae with blood flow.

Risks include age, smoking, vHL disease, dialysis. More prevalent in women.
Hematuria is seen in 60% of patients as well as weight loss, anemia, fatigue.
1% are bilateral at presentation and 1 more % will become bilateral on followup
10% are mutifocal (therefore mostly ipsilateral) at presentation

50% are hyperechoic to renal parenchyma. 40% are iso. 10% are markedly hyperechoic, nearly iso to the pelvic fat and can be confused with angiomyolipoma.
70% have calcifications, punctate, amorphous, mottled. The only unlikely type is peripheral rim-like

The solid lesion is usually very vascular with doppler flow, but the flow is still rarely as much as the normal parenchyma, and no detectable flow still doesn't rule out RCC.

Robson classification of RCC

I - involving kidney only
II - involving the prenephric fat also
IIIa - has invasion of the renal vein
IIIb - involvement of regional nodes
IVa - has invasion of adjacent organs
IVb - has distant mets

Medullary renal cancer

is a variant of RCC that occurs almost exclusively in people with SC trait (not disease, just trait)
Is more agressive, and therefore the ave population is younger than for just regular RCC

Differential of a solid renal mass

Transitionalc cell CA
Juxtaglumerular CA
Column of Bertin
Focal parenchymal hypertrophy
Focal pyelonephritis

Transition cell CA in the kidney

makes up over 90% of urethelium based tumors (the rest are squamous type)
Commonly multifocal and bilateral. 10% have metachronous or synchronous primary kidney tumor.

Most are too small to detect by US exam.
Classic appearance is of urothelial thickening or a mass in the renal pelvis.

Differential includes a blood clot, fungus ball, fibroepithelial polyp, malakoplakia, calcli.
Can be mistaken for a prominant renal papulla (filling defect in a calyx)

Lymphoma in kidneys

Usually only occurs as part of pidespread systemic disease due to lymphatic or direct spread.
Usually bilateral since late in severe disease
Mostly this in non-Hdgkin type
Usually adymptomatic. Kidney function preserved for a long time
Most common US appearance is bilateral hypoechogenic masses. Unilateral and unifocal types are rare.

Some are nearly anechoic and can be mistaken for cysts, but the have no posterior enhancement (absorb sound rather than transmit it)

Mets to kidneys

Most common sources are lung, colon, breast, gastric, prostate, pancreas and melanoma
Unusual for these to be complex or cystic. Most commonly these are mutiple solid lesions.

Angiomylipoma of kidney

Consists of vessels, muscle and fat.
Most patient are middle age and female
NO malignant potnetial. Symptoms are rare
Can remorrahge, whis rare.
Usually < 4 cm diameter
Clasic US appearance (seen in 80%) is homogeneous well-defined cortical mass as echogenic as renal fat, but such a lesion has 10% chance of being RCC
Can have acoustic shadowing (which is NEVER seen in RCC)
Almost never has cystic component (as opposed to RCC)
Further imaging includes CT or MR to look for gross fat signal.

Differential includes RCC, deep cortical scar or cysts filled with crystals (in which case may have ringdown artifact)


Is a type of adenoma. Overall 5% of renal masses
US appearance is nonspecific. Can have a stellate scar, but difficult to see even with a contrast study and even then is similiar to necrosis or hemorrhage that can be seen in RCC. Therefore these are always removed for pathology

Juxtaglomerular cell tumor

Is rare, and benign. Also known as reninoma since it actively secretes renin
Prototypical patient is a young woman with severe HTN

US appearance is variable, usually hyperechoic mass

Multilocular cystic nephrom

is a benign, well encapsulated tumor consisting of myltiple cystic spaces.
Tends to effect young boys and old women (michael jackson tumor)

Differential includes cystic RCC, cystic Wi;ms tumor. Therefore always removed for pathology


Infection secondary to statis or hemorrhagic seeding
White cell casts in tubules cause microscopic obstruction that is patchy, with a well defined border and extends to the cortex, causing decreased function and ischemia.
Chronic scarring can occur.

US findings usually normal in cases of uncomplicated pyelonephrits. Sometimes the kidney can be enlarged. Sometimes there are areas of increased or decreased echgenicity.
Role of US is more to look for complications such as obstruction, abscess and calculi

Renal abscess

Complex renal or perirenal fluid collection
A large one should be drained
Small ones can be tried on course of ABx first

Don't conduse with hypoechoic fat (usually bilateral asn associated wtih renal atrophy)

Xanthogranulomatous pyelonephritis

Chronic inflammatory precess in setting of chronic obstruction
Most common causes are Proteus and E. coli
>75% have a staghorn calculus
Classic triad of staghorn calculas, renal enlargement and lor renal function

On US look for a shadowing stone, dilated renal calices and perinephric inflammation

Emphysematous pyelonephritis

Very serior complication
Usually happens in diabetic women.
Cuased by gas forming organisms such as E. coli, which thrive on the high glucose.
Nephrectomy is the usual required treatment.

Emphysematous pyelitis

Less serious than emphysematous pyelonepritis, involving only the collecting system.
On Us look for right gas reflection with dirty shadowing or ringdown artifact.

Complex renal cystic masses

Hemorrahgic cyst
Infected cyst
Multisptated cyst
Cystic RCC
Multifocal cystic nephroma

Causes of urothelial thickening

Ureteral calculus
Ureteral stent
Relieved obstruction
Transplant rejection
Transplant ischemia
Transitional cell cancer

Renal calculi

US appearance depends on size, not composition.
Larger stones are echgenic and shadowing.
Smaller soned are still echgenic, but have no shadow.
Doppler imaging can produce color ringdown artifact "twinkling"
False positives can occur with renal vascular calcification (usually linear or focal beads in linear arrangement)

US detenction sensitivity is better than CR but worse than CT. Over 5 mm, sensitivity is very good, <5 mm not good.

Best seen in the proximal ureter, the ureteropelvic junction and distal ureterovesical junction


Very well imaged by US. Changes can be seen before calcification is dense enough to be seen on CT
Appearance is of increased medullary echogenicity

Renal parenchymal disease

US usually shows increased cortical echogenicity greater than liver equal or greater than spleen.
Echogenicity corelates to severity of disease
Role of US is to look for obstruction and assess renal size

Renal trauma

US not a good modality for this. CT is far superior as hematomas are very difficult to see on US.

Renal arteyr stenosis

Accounts for only 5% of HTN cases, nevertheless is important to find since this is curable

US doppler findings include
Focal aliasing or fical tissue vibration
Peak systolic veolocity over 200 cm/sec
Peak renal/peak aortic systolic flow ratio over 3.5

Like to have the patient fast before exam to take bowel out of the picture.
Proximal stenosis causes blunting of wave form distally. Measure this with early systolic acceleration. Less than 500 cm/sec squared is abnormal

Doppler can not tell between hgih grade vs complete stenosis or borderline stenosis

Differential includes FMD and atherosclerosis

Renal vein thrombosis

Bland thrombus is rare in adults
Usually secondary to dehydration, coaculopathy, trauma, renal parenchymal process causing nephrotic syndrome (such as membronous glomerulonephritis), or secondary to IVC or gonadal vein thrombosis extending into the renal vein

Imaging depends on acuteness and completeness of thrombosis
In total occlusion the kidney is enlarged and there is no venous flow on doppler. There is decreased arterial flow with high resistance pattern and possibly diastolic reversal.

Clot usually develops slowly allowing collateralization, which which case the kidney is normal size and arterial flow is normal. Therefore detection of venous or arterior flow does not exclude venous thrombosis. Look for the filling defect.

The left renal vein is difficult to image since it is long and there is a lot of overlying bowel, but can not excluded thrombus unless the whole thing is seen.

Pseudoaneurysm of kidney

Usually secondary to trauma
On US appears a cystic space.
Best imaging is with doppler which shows internal swirling ro to-fro internal flow.
Pseudocysts are common post transplatn
Often associated with arteriovenous fistula, in which case the flow is low resistance high veolicry from the artery, into the pseudoaneurysm and out to the vein.

Arteriovenous fistula

Usualy secondary to trauma. Small one are common post biopsy but these are usually asymptomatic.
Large ones can cause CHF (rare) are renal HTN.
Most resolve spontaneously. Persistently symptomatic ones are embolized.

Kidney transplant US eval

Look for hydronephrosis, free fluid, vascular stenoses.
Mild renal pelvis distention is normal post transplant and peritransplant fluid collections are also very common.
A small hematoma, seroma etc is not particularlyl important.
A large collect is important in the sense of mass effect that can constrict the ureter, kidney parenchyma or vessels.
Lymphoceles are MOST common 1-3 weeks out.
Urinomas usually are seen in the first 2 week post procedure, usually at anastomosis site and therefore close to the bladder with mass effect on the bladder.
Abscess looks similar to all the other fluid collections

Transplant rejection, kidney

Causes swelling of parenchyma and urothelium
- can see enlarge and hypoechoic pyramids
- pathcy cortical hypoechogenicity
- decreased visibility of renal sinus
- Increased resistive index
- the more of these findings are actually present, the more likely rejection.

Differential includes acute tubular acidosis, cyclosporin toxicity, infection


spares lymph nodes, predominantly affects organs
Kidney is actually less likely to be involved
look for masses in the liver, lung and spleen
also solid hypopechogenic infiltration of soft tissue around the transplanted organ

Tested US anatomy

Major arteries are peripheral. The capsular arteries branch then head centrally (hence centripetal arteries). In 50% at least one branch goes in through mediastinum


Most common scrotal mass
represents the head of the epididymis filled with sperm and fluid
There are low internal echoes

Epididymal cyst

Can occur in the head tail or body
Contains serous fluid
Nearly anechoic and indistinguishable from spermatocele (meaning any time spermatocele is in differential, so is a cyst)


Same as a hydrocele but occuring in the spermatic cord.
Pyoceles and hematoceles are considered complicated hydroceles.
Appears with complex internal echoes and sptation often with scrotal wall hyperemia


Collection of dilated veins
85% are on the left, likely secondary to compression of the left renal vein by SMA
Remaining 15% are mostly bilateral
Isolated right varicocele is rare and compression due to a mass should be suspected in every case

Even a small varicocele can cause infertility
Usual location is lateral posterior and/or superior to testis
Upper limit of nl scrotal vein diameter is 2 mm
Flow is usually too slow to detect
Valsalva maneuver causes dilation and detectoable retrograde flow into the varicocele

Non-neoplastic peritesticular masses

Exuberant scar
Sperm cell granuloma
Chronic hematoma
Scrotal wall edema

Intratesticular cyst

Is overall much less common than a spermatecele
Usually occurs in the elderly
Located near the mediastinum
Seen on up to 10% of US exams
If multiseptated suspect malignancy-do further workup

Tunica albuginea cyst

Is a varian of testicular cyst, but this one is very firm and palpable, typically solitary and small
Always at the periphery (cause that's where the tunica is)
Ignore it if simple.

Testicular neoplasms

Germ cell Stromal
Seminoma Leydig cell
Embryonal cell Sertoli cell
Choriocarcinoma Lymphoma
Yold sac Mets
Mixed germ cell Epidermoid cyst

Tubular ectasia of rete testis

Another cystic appearing thing
Usually there are bilateral mediastinal changes
Often associated with spermatocele and intratesticular cysts

On US, multiple small cystic or tubular structures are seen in the mediastinum, pathognomonic

Germ cell tumors

Most common testicular tumor in a young man
Pure seminoma and mixed are most common.
10% present with pain
In elderly, mets are much more common than primary neoplasm.


US appearance is homogeneous, hypoechoic when small and heterogeneous when large.
Calcification and cysts are rare
Radiation sensitive with good prognosis (therefore important to detect)

Mixed germ cell tumor

Combination of seminoma, teratoma, embryonal, choriocarcinoma cell lines
Usually heterogeneous with frequent calcifications and cysts
Most have detectable internal vascularity and some are hypervascular.
Scan the retroperitoneum around the kidneys for nodal mets if a germ cell tumor is found.
Conversely, if one finds retroperitoneal adenoapthy ina young male, look for a testicular germ cell tumor.

Non-germ cell tumors

Most common are Leidig and Serotli, which make up 5% of testicular tumors overall
Most are benign, but are active hormone secretors, so present that way.
They are always removes for pathology, because they can not be differentiated from other neoplasms; variable echogenicity, but usually homogeneous within a particular tumor, with detectable vascularity

Testicular tumor mimicks

Focal orchitis
Testicular atrophy, focal
Adrenal rest


Tiny non-shadowing focal reflection representing calcification in seminiferous tubules
5 or more are needed in one image to diagnoses this condition
If <5 are seen on all images, then call it limites testicular microlithiasis
Associated with tumors among many other things (~10%). No regular US screening, patient should do regular self exams

If 1 tested has a tumor and the other demonstrates microlithiasis, biopsy is indicated, since risk for CA is definitely elevated on the microlithiased side

Tunica albuginea plaque

is calcification of the tunica
Presents as palpable mass
Usually is secondary to prior trauma or inflammation

Testicular torsion

Results from poor fixation of the tested in the scrotum
The most common cause is bellclapper deformity where the tunica completely surrounds the testes, and there is no attachment to the scrotum
Infarction occurs after 4 hours with high degree of torsion. With low degree (180-360 degrees) or intermittent can be saved upt to 24 hrs.

If the testis looks normal, its likely ok regardless of duration of torsion
If the tested is hypoechoic or heterogeneous, likely infarcted, regardless of duration or degree

On Doppler imaging, look for decreased asymmetric flow. Also look for a hyperemic scrotal wall secondary to inflammation

False negatives are due to low grade, intermittent or spontaneously resolved torsion


The epididymus is enlatge and hypoechoic
When advances, microabscesses can be seen, and fluid collections
Often found in association with orchitis. Isolated orchitis is rare (usually mumps)

Differential includes torsion, diffuse lymphoma or leukemia, diffuse seminoma


Isolated orchitis is rare (usually viral, mumps)
instead it is common to find orchitis with epididymitis.
The testes is enlarges, hypoechoic with increased flow

Testicular trauma

Lood for discontinuity of the tunica albuginea
If the tunica is intact, usually no surgery is necessary.
If ruptured, surgery required within 72 hours

Bladder sono

The most connom abnormality is wall thickening
Usually secondary to outlet obstruction, followed by neurogenic, inflammation leading to edema, radiation and neoplastic causes
The upper limits of normal wall is 3 mm distended and 5 mm collapsed

Tumors of the bladder are 90% transitional cell type. Risks include soming analgesics, industrial carcinogens
5% of tumors are squamous cell, usually secondary to schistosomiasis, neurogenic bladder and chronic inflammation
2% are adenocarcinomas-these are usually in a uruachal diverticulum

Transitional cell carcinoma

Majority arise at the posterior wall (trigone)
On imaging the mass is polypoid extending into the lumen, less often infiltrative in the wall.
Differential includes blood clots, stones, fungus ball, inflammatory process, invasice tumor from adjacent organ, wall trabeculation, BPH, endometriosis, malakoplakia, leukoplakia, TB, schisto and the rare tumors (squamous and adeno)
To confirm CA, look for the mass to be immobile with internal vasculature

Bladder diverticula sono

Usually secondary to outlet obstruction and often found in association with wall thickening.
To detect flow in the connection, compress the bladder with the transducer.
Stasis in the diverticulum predisposes to stones, inflammation and cancer.

Uracah diverticulum

Occurs and the anterior dome.
Predisposes to adenocarcinoma

Bladder wall lesions

Primary neo Secondary neo
Transitional cell Rectum
Squamous cell Prostate
Adenocarcinoma Cervical
Pheochromocytoma Uterine

Inflammatory Other
Diverticulitis Ureterocele
Crohn's Urachal cyst
PID Cystitis cystica
Appendicitis Endometriosis


Is a dilation of intramural portion of distal ureter. The bubble prtrudes into the bladder lumen
On US, looks like round/oval thin wall cyst on the posterior wall.
Can be seen filling and emptying in real time.

Urethral sono

Ultrasound really godd only to evaluate diverticula
Appears as afluid collection adjacent to the urethera
Usually start at mid-urethra and extend posteriorly, frquently wrapping around the urtethera.
Complications include stones and cancer

Penis US

Used to evaluate dysfunction
Usually a vasoactive compound is injected into corpus cavernosum then blodd flow is assesed. Normal is 35 cm/sec or more. 25 or less is arterial insufficiency. 25-35 is indeterminate


Look for an arterial venous fistula, commonly secondary to trauma (high flow) or thrombus of a dorsal vein (low flow)

Peyronie's disease

Fibrosis of tunica albuginea of corpora cavernosa
Idiopathic, usually in men over 45
The penis bends to the affected side secondary to lack of tunica compliance.
Pain can make intercourse impossible
Ultrasound demonstrates focal tunical thickening

Prostate CA

Is the most common malignancy in men and second most common cancer mortality cause
Frequency greates in black men, then white then asian
Most are clinically occult. 50% of men over 50 and 80% of men over 80 have foci of prostate cancer
70% occur in the peripheral zone, only 5% in the central zone, 20% in transitional (even though it is the smallest)

Ultrasound appearance is variable. 70% hypoechoic to periphral zone parenchyma, the rest are hyperechoic or mixed.
Can be discrete or infiltrating. Cystic change is very rare.

Pancreas sonon anatomy

Head should be 3 cm or less
Bone 2.5 cm or less and tail 2 cm or less
Pancreatic duct should be smooth. The upper limits 3mm for the young, and increases with age.
Echogenicity is greater than liver buc can be higher or lower than spleen

Acute pancreatitis sono

On CT this can look normal
On US, pancreas can be hypoechoic or heterogeneous. Best way to tell is compare to liver (but beware of comparing to fatty infiltrated liver)
Vascular complications include thrombosis of plenic vein, SMA or extention to plrtal

Cystic pancreas lesions

von Hippel Landau
Mimicks like totuous vessels, anurysms etc.

Chronic pancreatitis

Pancreas calcification is a classic sign
Look for multiple, punctate bright reflector foci with or without shadowing.
Most commonly seen with cases causes by EtOH, less so with pancreatitis resulting from gallstone impaction
The duct is often dilated with dhort strictures giving "chain of lakes" appearance.
HOWEVER, both patterns are also seen with cancer.

Pancreatic cancer

Adenocarcinoma areises from ductal epithelium. ameks up more than 90% of all pancreatic tumors
1 yr survivial rate is 10%, median is 3-8 months
Most occur in the pancreatic head. Initial presentation usually painless jaundice

On US, most are a hypoechoic mass as compared to adjacent pancreas.
There may or may not be distortion of the local anatomy
Commonly there is obstruction of the CBD with abrupt cutoff.
There may be atrophy distal to the tumor

CT is best modality to evaluate. US is useful for equivocal cases or for mets and involvement of adjacent vessels, invasion and ascites

Hypoechoic pancreas lesions

Pancreas CA, focal pancreatitis, lymphoma, mets, islet cell tumor, thrombosed aneurysm

Islet cell tumors

When multiple, associated with MEN I
Insulinomas make up 70-75%.
Usually solitary, <2 cm and 95% are benign
Can be anywhere in pancreas
Syptoms secondary to high insulin
Gastrinomas make up 20%
Mpst are malighnant
40% have mets on presentation
Symptoms are secondary to gastricn leading to peptic ulcers, secretory diarrhea
When nonfunctioning presents when the mass is already large, with mets

Cystic pancreas neoplasms

Make up less than 5% overall
includes microcystic adenoma and macrocystic adenoma

Microcystic adenoma

(aka serous cystadenoma)
is benign, prototype patient is meedle age to elderly woman
Well circumscribed, susually large (mean 10 cm) with multiple small c ysts
Can have central stellate scar tha may calcify

Sono appearance varies
If cysts are tiny, can look like a solid hyperechoic lesions
When cysts are 5-10 mm looks multicystic
Generally the cysts are less than 2 cm diameter and more than 6 are seen for this diagnosis.

Macrocystic adenoma

(aka mucinous cystadenoma)
Malignant vs malignant potential
Prototypically occurs in middle aged women
Usually in the body or tail of pancreas
Has well defined cysts with thick mucin, septations and mural nodules
There are occasianl mural calcifications
Sono clearly shows cysts, seprarions and mural nodules

Differential of cystic pancreas lesions

Microcystic and macrocystic adenoma, necrotic pancreas adenocarcinoma, adenocarcinoma with pseudocysts, solid and pappilary epithelial neoplasm, intraductal papillary mucinous tumors, PCKD, vonHippel Landau

Splenic cysts

Most are post-traumatic and represents full evolution of a hematoma (serum with pseudocapsule).
Wall calcification does not aoutomatically imply neoplasm
Also can represent hydatid disease
Pseudocysts from the panrcreas can erode into the spleen
Other perisplenic cysts include exophytic renal, endometriomas and mets from ovarian CA

Splenic hemangioma

Common in the spleen but not usually seen on imaging, and is more variable in appearance than liver hemangiomas

Lymphangioma splenic

Seen as multiple cysts when they get large enough
If cysts are very small, can look solid hyperechoic


Can be focal multifocal or diffuse
Then focal, usually is hypoechoic, and heterogeneous when large. Sono not a good choice to evaluate

Splenic mets

Uncommon overal and occur late in disease, usually by hemorrhagic seeding.
Melanoma has the most propensity to do this.
Things like lung, breast, colon are predominant overall due because they are so much much more common.

Appearance is very variable.
Avoid US guided biopsy since bleeding risk is very high

Splenic masses

can represent primary or secondary neoplsm
granulomatous disease
extramedulary hematopoiesis
Gaucher's disiase

Fungal abscess in spleen

Simila appearance to a liver abscess.
Usually a target lesion with hyperechoic center

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