|Fetal echogenic bowel||commonly found in 3rd trimester, uncertain clinical significance.|
When found in second trimester, can be normal or associated with
intrauterine growth retardation (IUGR),
bleeding, cystic fibrosis (CF),
congenital viral infections
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.
|IUP||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.|
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
|Gallstone||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
|WES|| 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
|Sludge|| 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|| Uncommon|
Melanoma has most "tendency" to do this, but still infrequent
|Adenomyomatosis|| 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|| Common:|
|Causes of gallbladder wall thickening|| Biliary:|
Cystic duct obstruction
Non-biliary, which is usually concentric:
Hepatitis causes marked thickening
|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|| Hematoma|
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|| Hemangioma|
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|
Small calc without mass
|Causes of diffuse hepatic enhomogeneilty|| Common Uncommon|
Mets Hepatic fibrosis
Farry infiltration Lymphoma
|HCC||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
|Schistosomiasis|| Rare in the US, but common worldwide|
The infection is in periportal tiss, resulting in thick portal triads.
|Hepatitis|| 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 |
Cirrhosis Portal thrombus
Fibrosis Hep vein thrombus
Lymphoma IVC abstruction
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|| Ascited|
Increased diameter of the portal vein, 13 mm
Increased size of hepatic arteries
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
|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
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
|Choledocholithiasis||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.
Easily onfused with bilary gas. With gas there is often ringdown artifact. Stones don't ring.
Bacterial infection (enteric)
Recurrent pyogenic cholangitis
Flukes lead to bacterial infection leading to stones
|Cholangiocarcinoma||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
|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|
Obstructed upper pole
|Peripelvic cyst|| Likely lymphatic ductule in origin|
No communication to collection system or vasculature
Ofetn bilateral and multiple
|US of PCKD||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
|RCC||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|| RCC|
Transitionalc cell CA
Column of Bertin
Focal parenchymal hypertrophy
|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)
|Oncocytoma|| 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
|Pyelonephritis||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|
Multifocal cystic nephroma
|Causes of urothelial thickening|| Pyelonephritis|
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
|Nephrocalcinosis|| 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
|PTLD|| 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|
|Spermatocele|| 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)
|Funicocele|| 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
|Varicocele||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|| Spermatovele|
Sperm cell granuloma
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
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.
|Seminoma|| 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
|Microlithiasis||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
|Epididymitis|| 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
|Orchitis|| 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
Crohn's Urachal cyst
PID Cystitis cystica
|Ureterocele|| 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
|Priapism||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|| Pancreatitis|
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
|Lymphoma|| 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|
|Fungal abscess in spleen|| Simila appearance to a liver abscess.|
Usually a target lesion with hyperechoic center
|Granulomatous disease of spleen|| Usually TB or Histoplasmosis, they look the same|
Appearance usually mutiple hyperochoic foci representing calcifications
Sarcoid has a different appearance-diffuse or multifocal hypoechoic masses
|Solid spleen lesions|| Hemangioma|
Glycogen storage diseases
|Splenosis|| Occurs usually after trauma = implantation of splenic tissue on intraperitoneal surfaces with viscularization and growth of macroscopic nodules|
Nodules look like spleen-homogeneous, round/oval
Differential includes intraperitoneal mets, endometriosis. Look for history of splenic trauma
|Splenic infarct|| A common cause of splenic lesions|
50% are multifocal
Usually hypoechoic with coarse texture
Scarring can make the lesion hyperechoic over time
|Bowel sono anatomy||normal well thickness is less than 5 mm|
|Bowel wall thickening|| Inflammation (diverticulitits, crohn's, ischemia, pseudomembranous colitis, ulcerative colitis) infarct, neoplasm, ischemia, edema, hemorrhage|
If eccentric; carcinoma lymphoma, GI stromal tumor, ulcer, intususception
|Intususception|| In adults look for a lead point such as a polyp, lipoma, stromal tumor, lymphoma, mets, sprue, mecke's diverticulum|
If no blood flow on doppler, there is increased risk of necrosis.
|peritoneal mets||Sources include Gynecologic tumors, GI, pancreas, bronchogenic CA and breast CA|
Often they are very small and not detectable by US.
Once up to 1 cm diameter, the can be seen on US and CT.
Typically they are hypoechoic soft tissues nodules just deep to the abdominal wall
They are spherical and don't communicate with bowel and don't move
Ascites is also often seen
|Pseudomycoma peritonei|| Mucinous tumor implant from ovary or GI (appendix)|
Ranges from loculated anechoic fluid collection with mass effect to septated collection with or without internal echoes to a hyperechoic mass with or without calcifications
|Omental infarction|| Most common in men, and mostly on the right|
Edema of omentum results in echogenic mass with marked sound attenuation
|Sneumoperitoneum||Free air - bright reflector with dirty shadowing and ringdown immediately deep to the deep fascia|
|Peritoneal masses|| Mets|
|Abdominal wall masses|| Mets|
|Abdominal wall hematoma|| Usually post-traumatic (surgery etc.)|
Below the arcuate line become bilateral, and above remains unilateral.
Complex appearance of a mass with slid and liquefied areas
Usually the shape is lenticular
|Abdominal wall neoplasm|| Most are mets, usually round, hypoechoic|
Differential includes desmoid, endometrioma, lu=ymphoma, lipoma, complex fluid (hematoma, abscess)
|Hernia|| Occurs in up to 50% of men lifetime|
Incisional hernia is seen as a fascial defect
Direct inquinal arises inferior/medial to inferior epigastric artery
Indirect arises superior/lateral and travels anterior to the artery
|AAA sono||95% occur below the renal arteries|
Normal aortic diameters are 2.5 cm at diaphragm, 2.0 or less at midabdomen down to 1.8 at the bifurcation.
Measure the aneurysm from outer wall to outer wall (this corresponds to what the surgeons see)
Distention is considered aneurysmal when the diameter is 3 cm or more. If more than 2 but less than 3, call it ectatic.
Surgery indicated when 5 cm or more, or rapid enlargement (>1 cm/year) due to high risk or rupture
Atherosclerotic aneurysms are usually fusiform.
Saccular aneurysms are usually mycotic or pseudoaneurysms
Thrombus may contain crescentic hypoechoic foci = liquefied clot)
|Aortic dissection on sono|| Really US is not good for this purpose.|
The flap can be seen when it is perpendicular to the sound beam and foppler can resolve sual luman flow, but it is difficult
|IVC sono|| Thrombus can extend from ovarian vein, renal vein etc.|
Tumor thrombus can come in from RCC, HCC, primary adrenal tumors.
Most common primary tumor is leiomyosarcoma from the wall. It is very rare
|Adrenal sono|| Sono does not image adrenals well, particularly the left because it is deeper.|
Adrenals are the 4th most common site of mets overall
|Adrenal mass|| Adenoma|
|Source of mets to adrenals|| Bronchogenic carcinoma has particular predisposition|
Indistinguishable from adenoma, usually larger and heterogeneous
|Adrenal adenoma||Usually <3 cm. Homogeneous on sonography, isoechoic to normal liver|
|Adrenal pheochromocytoma|| Arises from adrenal medulla most of the time|
the rest of the time from sympathetic chains
Mass is usually large, vascular, heterogeneous
Rarely can be predominantly cystic
|Primary adrenal carcinoma||Very rare|
Bimodal age distribution, children or elderly
Typically mass is large with symtpoms secondary to mass effect on adjacent organs.
14% are hyperfunctioning leading to Cushing's syndrome
Necrosis, hemorrhage and calcifications are common.
There is propensity to invade veins, progressing to the cava.
|Non-Hdgkin lymphoma of adrenal|| Involvement of the adrenals is not uncommon in systemic disease|
Usually happens by direct invasion
Up to 50% are bilateral
Typical appearance is solid hypoechoic
|Myelolipoma|| Benign tumor|
Sono appearance is usually hyperechoic secondary to the gross fat component
|Adrenal hematoma|| Usually secondary to trauma, surgery, coaguloapthy, spesis, severe stress, hypotension or tumor.|
Looks like any other hematoma (variable, lacy etc.) and follows normal hematoma evolution
|Thyroid sono||Normal thyroid is homogeneous, hyperechoic with scattered vessels. AP diameter of the lobes is 2 cm or less. AP diameter of the isthmus is 4 mm or less|
|Nodular hyperplasia|| Most common cause of thyroid nodules|
Nodules frequently have a cystic component, often with internal septations and mural nodules
Bright internal reflectors represent colloid
|Benign follicular adenoma||makes up 5-10% of thyroid nodules|
Some may be autonomous functioning
There are often found in association with other nodules rather than isolated
Typically appear solid but either hyper or hypoechoic
Often these have a hypoechoic halo
A minority have a well defined cystic component
These can not be destinguished from follicular CA and therefore always biopsied and resected
|Papillary thyroid carcinoma||Most common thyroid cancer|
Accounts for about 75%, followed by follicular, medullary, anaplastic and hurthle cell
Pappilary is more likely in patients under 40, all the others are seen mostly in elderly
Mets to cervical nodes are often seen on presentation. Distant mets are rare
Mass is typically hypoechoic and entirely solid
Microcalcifications are secondary to salts deposition in psammoma bodies (looks like colloid reflectors)
There is a microcalcific variant, presents as a sclerosing focus less than 1cm diameter. There are lerge mets to cervical nodes without clinical evidence of a thyroid primary (nonpalpable I guess?)
|Follicular thyroid ca||makes up 10% of thyroid cancers overall|
Prototypical patient is a woman in the 50s
It spreads via lymphatics
There are minimally and widely invasive forms.
Mets to the neck are rare (compare to pappilary) whereas distal are seen in 20-40% of widely invasive form and in 5-10% of minimally invasive forms
Frequently coexists with multinodular goiter
Microcalcifications and nodal mets are NOT present (again as opposed to pappilary)
Overlaps follicular adenoma in appearance
|Medullary thyroid ca|| arises from C cells and secretes calcitonin which may be used as a serum marker|
20% are associated wtih MEN II
Is agressive and does not respond to chemo or radiation
Sono appearance is usually hypoechoic solid mass
Microcalcifications are common both in the primary mass and in the mets.
|Anaplastic carcinoma|| Rare under 60 years old|
The prognosis is grim
The mass is large and solid, hypoechoic
Local invasion is common at presentation
|Thyroid involvement of lymphoma|| Can be primary from systemic disease, usually non-Hdgkin type|
More in women, usually elderly
Mass is rapidly growing, large, solid, hypoechoic
Infiltrates the thyroid widely
|Mets source to thyroid|| Lung, breast, RCC.|
No specific songraphic appearance
|Thyroid nodule characteristics|| Benign Malignant|
iso or hyperechoic Hypoechoic
Eggshell calcs Microcalcs
Colloid Cervical adenopathy
|Hashimoto's thyroiditis||Most common cause of hypothyroidism in US|
Peak age is 40-60 years, women 6x more than men
On sono the thyroid is normal or enlarge, hypoechoic
Normal homogeneous tecture is replaced with heterogeneous
There are thin echogenic fibrous strands causing multinodular appearance
Often the gland is exteremely hypervascular
There can be nodules
In the endstage the gland becomes atrophic
|Graves disease|| Most common cause of hyperthyroidism in the USA|
sono not used commonly for evaluation
Appearance is similar to Hashimoto-enlarged hypoechoic hypervascular gland
|DeQuervain's thyroiditis|| Subacute granulomatous thyroidits, may be viral|
The gland is enlarged and painfull. associated with fever. Often occurs post URI
On US, there are poorly marginated hypoechoic areas.
Serum thyroid level is normal or possibly low
|Hyperparathyroid on sono||men 2.5 x than women. Peak age 40-60, 85% are secondary to solitary adenoma|
On US adenomas are hypoechoic, homogeneous, hypervascluar solid masses
True cystic changes are rare
Usuall the mass in ovoif in the longitudinal axis
Most are just posterior to the thyroid
When in mediastinum, they are usually anterior to the thymus.
If IN the thyroid, they are usually in the posterior half of the gland and easily confused for a thyroid lesion
False positives include posterior thyroid septation, nodules, esophagus, longus coli muscle, veins
|Ectopic parathyroid adenoma|| Usual locations include low neck, mediastinum, retrotrahceal/esophageal, carotid sheath, intrathyroid|
Alternative imaging modality is sestamibi scan.
Preop imaging is not really necessary though, surgical exploration has a high success rate
|Carotid sono anatomy||The normal wall is seen. Blood is anechoic. There is a reflection line at the interface of wall and blood.|
Normal wall thickness is 0.9 mm or less. Thickness increases with atherosclerosis and corelates with risk of MI and stroke
ICA has a low resistance pattern
The ECA has a high resistance pattern
Another way to tell the ECA is to tap the temporal and see vibration in the ECA.
The CCA flow has characteristics of both high and low resistance.
Velocity increase in minor if stenosis is ,50%, then rapidly increases over 50% stenosis.
Peak systolic velocity is underestinated when there is an occul proximal stenosis, low cardiac output or aourtic stenosis
Overestimated with there is occlusion of the contralateral side
In these situations look at the ICA.CCA ration, end diastolic velocity.
Volicty rapidly drops again when stenosis gets clode to 100%
|ICA velocities|| stenosis psv ICA/CCA EDV Plaque|
none <125 <2.0 <40 none
<50% <125 <2.0 <40 <50%
50-69% 125-230 2-4 40-100 <50%
>70% >230 >4.0 >100 >50%
near occlusion variable visible
total occlusion None None None visible
|Collaterals for carotids||Most common pathway is from the cntralateral ECA through the head and neck to the ipsilateral ECA and then retrograde to the ICA via the bifurcation|
|Plaque|| Homogeneous throught thought to be stable|
Inhomogeneous, especially with hyoechoic defects (intraplaque hemorrhage) is unstable
Roport any identified plaque ulcerations - high risk
|Vertebral arteries||Reversed flow seen when there is stenosis at the origin of the subclavian|
|Jugular vein|| Flow should be monphasic|
Flattened fow shoudl raise supicion of central thrombus or obstruction - same goes for the subclavians
Thrombus is non-compressible on grayscale
Look for adjacent inflammation and hyperemia
|Chest sono||Ultrasound can actually be used for chest e.g.|
Can detect as little as 3 ml of fluid in the pleural cavity
Can not distinguish transudate vs exudate (but nother else can either)
Can detect septations, consolidation and air bronchogram, peripheral masses, pneumothorax, especially at pleural surfaces due to loss of normal comet tail artifacts
|US of tendons||Useful for rupture|
The end of a ruptured tenson is blun on long view and there is loss of architecture or it may nor be seen at all
Normal tendon is hyperechoic when perpendicular to the beam, otherwise hypoechoic
Same for ligaments
Muscle is hypoechoic with striation (no anisotropy)
Articular cartilage is anechoic to hypoechoic
Fibrocartilage is hyperechoic
Peripheral nerves are hypoechoic with fascicular architecture
|Tendonitis|| Due to inflammation or trauma|
Can see fluid distending the tendon sheath with or without thickening of the heath itself (which can be smooth or nodular if present)
The fluid can have low level echoes, especially if infected
|Rotator cuff on sono||Layers from deep to superficial are|
Humeral head, anechoic cartilage, echogenic cuff, hypoechoic bursa, hyperechoic peribursal fat, hypoechoic deltoid
Majority of tears are of the supraspinatus insertion on the greater tuberosity and can extend posteriorly to the infraspinatus, medial or both
Normal cuff does not compress
Torn cuff can be compressed because the sides of the tear slide apart and fat and muscle are pushed into the defect
On short axis view, if only the first 1.5 cm of the cuff posterior to piceps long head are involved, then its only thesupraspinatus. If more than 1.5 cm involved, then infraspinatus is involved also.
|Muscle tear classification|| I - limited number of fibers is torn|
II - the tear is more extensive with functional weakness
III - complete disruption of the muscle with retraction
|Bursa sono|| Normal bursa is not seen on US since it is a very thin potential space|
When fluid filled is it readily detectes, especialle around the knee
Most commonly evaluated bursa is Baker's cyst, which extends between the medial head of the gastrocnemius and semimembranosis tendon
|Ganglion cyst of the hand||Most common mass of the hand|
There are 4 typical locations
70% are at the scapholunate joint dorsally
20% are volar at the flexor carpi radialis
10% long the flexors of the digits sheaths
some small number are at interphalangeal joints - these are secondary to arthritis
All are anechoic and filled with thick mucin
|Giant cell tumor||Is secont most common mass of the hand.|
Same pathology as PVNS
Slow painless growth on the volar surgace of the fingers
The mass is solid and homogenous hypoechoic on US
It is adjacent to and partially surrounds the tendon, but does not move with the tendon
There is internal blood flow on the doppler exam
|Subcutaneous lipoma|| Echogenicity is variable, often not classically hyperechoic|
There may or may not be a capsule
The mass is compressible.
There is little if any flow
|Peripheral nerve tumors|| If the tumor is in the middle of the nerve, its usually a nerufibroma|
If the tumor is at nerve periphery, usually a schwannoma
Most are solid, hypoechoic, vascular
|Forign bodies|| All forign bodies are bright reflectors on US|
Galls and metal objects may have ringdown artifact
|Joints on US|| Effusions are anechoic unless septic, in which case there may be lowe lever echoes from debris|
Proliferative synovium is thick nodular with concentric thickening.
|Peripheral blood vessels|| At rest have high resistnace flow patern (triphasic with recoil post systole)|
After exercise the capillary beds open up and the flow becomes low resistance
|Venous thrombosis||Sequelae of thrombosis usually stabilize by 6 months post even|
There is eccentric vs diffuse wall thickening or wall calcifications
There may be irregular channels through partially recanalized lumen
Therefore it is recommended to repeat an US exam after 6 months to reestablish a baseline for tha affected vessel
|AV fistula||Proximal to the fistule tha wave form changes to a low resistance pattern due to easy runoff into the vein|
In the lower extremity, usually happens below the femoral bifurcaion
There is perivascular tissue vibration
Increased velocity is seen at the commynication site
Turbulen/arterial flow seen in the vein distal to the fistula
|Differential of tissue vibration|| Arterial stenosis|
AVF is usually much stronger then either of the above
|Fetal heart motion||Should always be seen by the time CRL reaches 5 mm on TV (6 weeks or so) or 9 mm on TA imaging.|
At 5-6 weeks gestation age hear rate should be 100 or more with 90 being the lowest limit (still has 25% loss rate even if normal heart motion is detected.
By 8 weeks should be 140-160 bpm with a lower limit of 120 and upper limit of 180
The most common arrhythmia is PAC. It is iteself benign but predisposes to spraventricular tachycardia
|Corpus luteum|| Most common adnexal mass|
Should be 3 cm or less
Resolves, usually by 12 weeks, but can be seen as long as 20 weeks.
|Gestation age determination|| In the 1st trimester the CRL is most accurate|
In 2nd trimester head measurement is more accurate than abdominal and can be used till about 20 weeks.
By the 3rd trimester the femur length becomes the most accurate landmark
|Lateral ventricles normal||To image tilt the probe cauded from axial to see the atria|
Atria should be constant size from 14-38 weeks and measurement is normally easily reproducible
Upper limits is 10 mm
10-12 mm is minimal ventriculomegaly. Follow-up closely
The choroid should fill 60-90% of the atria. In true enlargement, the percentage drops resulting in "dangling choroid sign"
|Normal cysterna magna|| An anechoic space just posterior to the vermis|
Normal range is 2-10mm
|Fetal stomach|| Should always be identifieable by 16 weeks gestation|
If not seen by 19 weeks with full 60 minutes of scanning it is likely abnormal
|Fetal kidneys|| Seen as early as 12 weeks and always seen by 17 weeks|
In the early 2nd trimester the renal pelvis is allowed to be up to 4-5 mm
In late 3rd trimester it is allowed to be 7-10 mm
IF caliectasis or ereterectasis is seen, any dilation is considered abnormal even if within the above limits
|IUGR||Fetal risk factors for IUGR include;|
Previous pregnancy with IUGR, structural abnormality, chromosomal abnormality, in-utero infection (TORCH), placental (infarct, abnormal cord, previa, abruption)
Maternal risk factors; Young, chronic hypoxia, HTN, collagen vascular diseases, DM, smoking, drugs.
US detection rate is about 70%
There are 2 mechanisms for IUGR
Malnutrition Decreased cell growth
Majority (90%) Minority
Detect in 3rd tri Detected early, 1st tri
secondary to malnutrition Head body and femur
of any cause are all affected
Asymmetric amniotic fluid is usually
Often oligohydramnios normal
|More on asymmetric IUGR||This is really due to starvation|
The body expends all resources on the head, leaving the body and extremities small
Subcutaneous soft tissue (fat) is lost first, the liver glycogen stores - which leads to sono appearance of decreased abdominal size
Eventually, if the starvation state persists then the entire fetus is affected
Often accompanied by oligohydramnios
|Biophysical profile|| 5 items|
Gross body movement
Each rated 0-2 with max total of 10
The first 4 are controlled from different regions of teh CNS, so give good overview of neural development
|Macrosomia||The fetus is asymmetrically enlarged with extra fat about the shoulders and body, increasing risk for shoulder dystocia|
Which can result in Erb's palsy from excessive traction at birth
Assicated with: maternal gestation diabetes or DM
Fetal weight is not predictive of macrosomia *never even mind the 15% error margin on the weight calculation
|Gestations sac||By transvaginal can be seen by 5 weeks, approximately 2 mm diameter at this time|
Grows about 1.2 mm per day
The sac is almost always seen by the time beta is 1800-2000. Only 50% are seen when beta is 1000.
The sac should be in the upper uterine body, mid-point between the wall.
Lower position may be OK or may represent impending abortion
Growth should be evaluated at least 5 days apart to avoid error
The embryo is usually first seen then the MSGD is 12 mm (= 6.2 weeks) and should always be seen by 16 mm diameter
By TA imaging the size and dates are later, usually 27 mm and 8.1 week age.
MSGD of 25 mm (by transvaginal) and no embryo is considered abnormal
Other factors suggesting abnormal sac: distorted shape, <2 mm decidual rim, hyperechoic rim, low position
|Embryo|| Should be seen by 6 weeks on transvaginal|
Heart and body should be seen at head and body should be seen at 8-9 weeks
Heart and vessels seen at 9-10 weeks
Spine and extremities at 11 weeks
|Gestational sac/embryo ratio|| To calculate this subtract the CRL from the mean gestation sac diameter|
Normal is >5 mm
Most fetuses that have <5 mm of space are aborted spontaneously because this is first trimester oligohydramnios
|Yolk sac|| Usually seen when MGSD is 8 mm by TV|
Failure to see the yolk sac is not considered abnormal, just give it time
|Vanishing twin|| Suggested when there is a second sac which is distorted and without an embryo|
Diagnosis can only be truly made if the 2nd embryo was seen at some point
The blighted sac should resolve by the 2nd trimester
|Hydatidiform mole|| Classic triad of presentation is an enlarged uterus, hyperemesis, elevated beta often over 100k (this can be normal in a normal gestation over 8 weeks, or with late 1st early 2nd abortion or mutiple)|
Differential includes: partial mole with hydrops (lower malignant potential)
50% of cases are associated wtih multiseptated cystic ovarian masses (theca lutein cysts) which are bilateral
|Ectopic pregnancy||Only 60% of women with extopic have a history of a missed period|
Classic presentation is irregular menstruation, bleeding, abdomina/pelvic pain, tender adnexal mass. ( of course not often found)
Risk factors: 1) Abnormal falopian rubes secondary to prior infection, developmental defect or surgery, 2) normal falopian tubes but with IUD, on induction therapy, delayed tubal transport or 3) history of prior ectopic
If the ectopic is in an expandable region like cornual or peritoneal, presentation is later than with tubular location, as late as 2nd or 3rd trimester
There can be an intrauterine fluid collection without normal fetal structures - this is a pseudogestational sac. It is usually abnormal, elongated because it conforms to the uterine canal
Even with a true ectopic - 10-20% of exams are normal.
Except in the extreemly rare case of heterotopic pregnancy, if an IUP is found, there is no ectopic pregnancy
Conversely if beta is positive but no IUP is found, ANY strange finding is suspicious
1) can see an actual embryo with heart motion (15% of TA and 20-30% of TV exams)
2) tubal ring or adnexal mass has a 95% predictive value
3) intraperitoneal fluid, especially with internal echous, the larger the worses and more predictive
Differential includes endometrioma, PID with or without abscess, hydrosalpinx, pyosalpinx, dermoids. None of these have a positive beta of course.
|Locations of ectopic pregnancy in decreasing order|| Fallopian (97%) usually ampullary, isthmus, fibrial, interstitial|
Uterine cornual (<5%)
|Heterotopic pregnancy|| Concurrent normal and ectopic pregnancy|
risk is 1 in 7k
|Decidual cysts|| simple cysts in the periphery of the endometrum,|
associated with increased risk in women with a positive beta but no IUP
|Interstitial ectopic||Implantation in interstitial fallopina (in the uterine wall)|
On exam there is absent or very thin layer of myometrium on the outer side of the sac. There is high risk of rupture and bleed
Look for the interstitia line sign - hyperechoic endometiral canal line abutting the sac at the top of the fundus, whereas the line would go around a normal sac (since its implanted in the wall)
|Fetal CNS|| All structures should be seen by 12-14 weeks|
Anencephaly_ on US no brain is seen above the orbits
Failure to identify the calvarium regardless of position-suspect anencephaly
Polyhydramnios is often associated, but may be normal since it builds up slowly
|Hydrocephaly||head enlargement is only occasionally present. Call it if the head is at least 2 weeks larger than the abdomen (presuming there is no IUGR)|
To identify hydrocephalus look for enlargement as above, an obstructing mass, lateral or 3rd ventricle dilation (3rd exceeding 3 mm transverse)
There is always at least a residual rim of brain tissue, which is important to identify to distinguish from hydranancepahly
|Microcephaly||Usually due to TORCH except T, developments (especially holoprosencephaly), genetic (especially trisomies), radiation, toxins or heavy metals|
Call it when BPD is more than 3 SD below the norm for gestational age (1SD is about 3 mm)
If BPD is 1 or 2 SD below normal, it can in fact still be normal
If the ventricles are also dilated there is likely loss of brain parenchyma
With periventricular calcifications suspect CMV
If there are calcifications in a normal size head, suspect toxo
|Holoprosencephaly|| There is frequent association with chromosomal abnormalities aspecieally trisomies 13, 18 13Q triploidy.|
Major formas include alobar, semilobar and lobar.
Head size can be nomral microcephalic or macrocephalic
Thalami and basal ganglia are typically fused
Facial anomalies are common
|Facial structures||Cleft lip/palate is the most common congenital facial anomaly|
Any part singly or in combination can be affected
Isolated involvement of the palate is usually not apreciated on in-utero scans
Eccentric or bilateral defects are more deforming and more often associated wtih other abnormalitis than central defect (trisomies, holoprosencephaly etc.)
|Micrognathia|| is associated with trisomy 13, 18, triplody etc usual suspects.|
True midline sagittal view is requred for diagnosis
|4th ventricle||Grows steadily with head size up to 8 mm at term|
|Cerebellum|| Grows steadily with head size|
It is fully formed by 10-18 weeks
Before that there can be a cleft between the hemispheres that the vermis fills in when it develops.
Therefore dandy walker malformation can not be diagnosed before 18 weeks
|Mega cysterna magna|| Megacisterna is a normal variant where the cysterna is over 10 mm in AP diameter but the vermis and the rest of cerebellum are all normal|
Differential includes posterior fosa arachnoid cyst
|Nuchal fold|| Measure this in the midline at 15-21 weeks|
Considered abnormal if over 6 mm
This does not apply after 21 weeks because then it naturally becomes thick
This is considered the most sensitive and specific in utero marker of trisomy 21. Detects about 1/3 of cases
|Nuchal translucency|| Measure this at 11-14 weeks|
An abnormally thick hypoechoic region along the posteior neck is highly corelated to aneuploidy, most commonly tri 21
Also associated with cardiac abnormality, diaphragmatic hernia and abdominal wall defects
|Choroid plexus|| Easily compressive, decreases in size when there is elevated intracranial pressure ( as with hydrocephalus)|
Also is a sourse of glycogen in fetus. If it is small, can mean malnutrition which can result in impaired brain development (but have to exclude hydro first)
|Choroid plexus cyst||Has association with trisomy 18|
Look for heart defects, abnormal feet (club or rocker), clenched hands with overlapping fingers, facial clefts, neural tube defects, radial ray abnormalitis and 2 vessel cord
If there is a cyst and anatomy is normal, triple screen is normal then fetus is likley normal. DO NOT do amnio
|Cystic structure posterior to thalami or brain stem|| Dandy walker|
Dandy walker variant
Dilated 4th ventricle
Vein of galne aneurysm
|Vein of Galen aneurysm|| Easy to see with Doppler - high flow with lots of turbulance.|
Also will se acrdiomegaly due to high flow CHF
|Germinal matrix hemorrhage classification|| I - hemorrahge contained in the germinal matric|
II - intraventricular extension of hemorrhage
III - Obstruction due to clots leads to hydrocephalus
IV - the hemorrhage extends into parenchyma
|AFP||a normal protein produced first in the yold sac then liver|
Is excreted by kidneys, found in amniotic fluid and maternal serum
Amnio level is highest in the 1st trimester. Maternal level is highest in 2nd trimester
Any open defect of the fetus elevates AFP, usually neural but abdominal etc also
False negative is very rare, usually due to a skin covered defect
False positives are common, up to 50% of cases
|Fetal spine|| Most should be seen by 16 weeks. At this time L5 is most caudad calcified vertebral body.|
The sacral vertebrae ossify at rate of 1 level every 2 weeks after this time.
e.g. fetus with S2 ossified is 16 weeks + 2*2 =20 weeks
|Neural tube defects||Most commonly occur in the lumbar region|
splaying of the posterior elements
defect of soft tissues
The actual sac (meningocele)
If there are thin strands in the sac, the nerve roots may be involved
The lower the defect, the better the prognosis
Also look for chiari malformation since there is high asociation between the two
Look for lemon sign, which for some reason in present in 98% of fetuses with a neural tube defect prior to 24 weeks, and then only 13% afterwards (keep in mind it is very nonspecific)
After 24 weeks the best sign is ventriculomegaly and obliterated cisterna magna
|Cysttic hygroma||On sono looks like spokewheel structure posterior to the neck (septations)|
Can be solitary or assciated with diffuse hydropic precess (in this case demise is highly likely)
60% are associated with chromosomal abnormality especially turner's, but also tri 21 and 18
Lymphoceles can occure anywhere in the body. In these other locations there is no associtation to the above abnormalities
|Sacroccygeal teratoma|| Interesting fact. This thing is never malignant while in utero, but can become malignant if not removed after birth.|
The risk becomes higher the longer it is left in
|Mass at the back of the fetal neck|| Cephalocele|
Cervical meningocele (rare)
|Fetal heart anatomy||The chambers of the heart are not seen before 16 weeks. At 18-20 weeks should be well seen. The liver is large at this time and elevates the apex.|
In the secont and third trimesters the atrial/ventricular size ration should be 1:1
The transverse diameter of AV valves should be 50% of the thorax or less
|Chance or detecting abnormality of 4 chamber view of the heart|| Frequent Infrequent|
Hypoplasticright ventricle Large ASD
Single ventricle TOF
AV defect Cardiomyopathy
Large VSD Svere aortic stenosis
Double outlet R ventricle Secundum coarctation
|Structural abnormalities of the heart|| Isolated right side defect is associated with other abnormalities|
So is rotation of the heart 0-90 degrees
|Disproportionate sice of the great vessels|| Large Aorta Small aorta|
Truncus arteriosus Hypoplastic left heart
Small pulmonary artery
Hypoplastic right heart
Ebstein's with pulmonary hypoplasia
|Fetal hydrops||Nonimmune hydrops categories:|
Cardiac primary failure makes up 22-40%
Can be high output type or myocardial
Myocardial type is secondary to severe arrhythmias, structural problems, myocarditis, AV shunts, twin twin transfusion
Decreased plasma oncotic pressure
From hepatitis (decreased production) or
Nephrotic syndrome (increased excretion)
Increased capillary permeability (anoxia, infection)
Obstruction of the venous return (congenital lesions)
Obstruction of lymph flow (turner syndrome)
Classic appearance is fluid in serous cavitis (ascites or effusions), skin edema/thickening, placental enlargement, polyhydramnios, possible hepatosplenomegaly (this is particuarly prominent with immune type),
Degree of abnormalities correlates to severity of hydrops
Hydrops with only skin thickening is rare and association with gestational diabetes,
isolated pericardial effusion is normal when it is <2 mm and even up to 7 mm is usually ok for the fetus
|Congenital diaphragmatic hernia||Most common intrathoracic extracardiac fetal anomaly|
Associated with abnormalilties of all other system, abnormal karyotype is seen in up to 56%.
Usually posterolateral (90% = Bochdalek type)
7x more common on the left, and usually unilateral
Usual US finding is gastric bubble in the left chest and none below the diaphragm
The heart is often pushed up or to the right
Bowel loops can be seen peristalsing in the thorax
Right sided hernia is difficult to detect as only the liver herniates, which is difficult to differentiate from the fluid filled lungs
Morgagni hernias are also very difficult to see by US for the same reason.
Obstruction of the bowel can mimick hydrops
Displacement of the heart can obstruct venous return
Prognosis is poor especially in cases where this is an isolated finding. The hernia continues to enlarge leading to pulmonary hypoplasia
|CPAM||Is a hamartomatous type lesions. Can occur anywhere in the lungs|
Usually it involves the only a sublobar area, involvement of the whole lung is less frequent.
Blood supply is either pulmonary or ectopic systemic.
I - Most common. Large cysts measuring 2-10 cm are clearly seen on sono imaging
II - cysts are usually <1 cm. If cysts are too small, the whole lesion can look hyperechoic solid.
III - Multiple bronchiole-like tubes <5 cm. Usually the whole lesions looks solid hyperechoic.
There is no significant association with other abnormalities including karyotype.
|Bronchopulmonary sequestration||Is less common that CDH or CPAM, only about 0.15% of pulmonary abnormalities|
There are 2 types, intraloabr and extralobar. The latter is more common
These are more commonly found in the lower lobes, more on the left and especially the posterior basal segment. Usually unilateral. Can be seen below diaphragm, but rare.
Most common appearance of sono is a hyperechoic mass at the lung base. Cystic component is frequent.
Extralobar type is often conical triangular and often presents with hydrops or pleural effusion
Extralobar supply is ectopic from thoracic or abdominal aorta.
This lesion can coexist iwth CPAM
|Laryngeal atersia|| Obstruction of the tracheobronchial tree (anywhere from larynx to bronchi)|
Usually bilateral. Unilateral is rare
Secretions can't be expelled. The lungs fill up with mucus and swell up compressing hte heart and depressing the diaphram
Can result in hydrops and other anomalies
|Pleural effusions in utero|| Are readily detectable. Usually are bilaterall|
There is association with hydrops
Unilateral is less frequent and associatited with focal conditions like a mass.
|Pulmonary hypoplasia|| The bronchial tree is fully developed by 16 weeks gestation|
Distal structures (alveoli) continue to develop til 8 years of age
Any error during this time results in pulmonary hypoplasia
|Pseudoascites|| A hypoechoic band between the fetal liver nad hyperechoic cubcutaneous tissues|
Represents the hypoechoic abdominal wall musculature. There is no actual fluid surrounding abdominal organs.
It does not extend deep to the tibs since the muscles insert on the bottom edge of the ribs.
|Intra-abdominal umbilical vein|| Thin parallel walls. Diameter is 3 mm at 15 weeks and 8 mm at term|
Varix = enlargement of the extrahepatic portion of the vein between the liver and anterior abdominal wall. Usually large and round.
Small association to hydrops, structural abnormalities, aneuploidy and 3rd trimester demise.
|Stomach location|| When the stomach is on the right, there is association with structural abnormalities, particularly cardiac.|
When the stomach bubble is in the thorax, most likelky represent a Bochdalek type hernia
|Gastric pseudomass|| There are echoes in the somach combining to look like a mass - in fact a normal variant|
More likely seen in fetus with slow transit, blood in the amniotic fluid after posterior abruption or amniocentesis
|Normal fetal stomach||Fill every 10-45 minutes and empties in 5 to 30 minutes|
If not seen or persistently <1 cm, rescan every 15 minutes up to 1 hour
If still not seen and amniotic fluid is normal or increased, there is likely inability to swallow.
If on the other hand there is oligohydramnios, likely stomach not expanding is a secondary phenomenon
|Esophageal atresia|| Most common type is associated with tracheoesohageal fistula|
Also associated with other abnormalities in 50-70% of cases (cardiac, espcially VSD in 25%, other GI in 28%, GU in 14%, CNS in 7%, facial in 6%)
Classic findings include polyhydramnios (60-90%) because fetus can;t swallow. The stomach bubble is absent
|Duodenal obstruction||is usually seen as the double bubble sign|
There is frequently polyhydramios
This is frequently missed (~50%) cause the typical findings don't develop til ~24 weeks gestation.
Intrinsic causes include atresis, diaphramatic web, and stenosis
Extrinsic causes include annular pancreas, malrotation and bands
Atresia is the most common (42% of cases) and has knkown association to trisomy 21. Therefore look for the other signs
|Lower GI tract obstruction|| Includes Jejunum ileum and colon. Jejunal obstruction is more common than duodenal|
On sono, normal loops of should not be over 15 mm long or over 7 mm in diameter.
Look for tripple bubble sign (jejunal obstruction)
|Fetal colon|| Grows from 5 mm diameter at 20 weeks to 15 mm at term. Upper limits is 20 mm|
In sencond trimester, the colon is echogenic and progresses to hypoechoic at term.
Meconium echo is variable/nonspecific
|Anorectal ateresia|| Associated with other abnormalities 75% of the time|
1) VACTERL vertebral, anal , cario, tracheoesophageal, renal, Limb syndrome
2) caudal regression, which includes renal agenesis/dysplasia, sactal agenesis, lower limb hyperplasia, sirenomelia (rare)
|Meconium ileus|| Occurs in up to 15% of CF infants - is the earliest finding of CF|
GI complications occur in up to 50% of these including valves, atresia, perforation, meconium peritonitis.
Proximal dilation doesn't occur til the 3rd trimester
|Meconium peritonitis||Is a sterile chemical inflammation|
50% is due to anderlying bowel disorder such as atresia, volvulus,, meconium ileus etc.
Idiopathic type may in fact be secondary to ischemia leading to perforation. The perf than heals spontaneously.
Look for intraperitoneal calcification (seen in 85% of cases) particularly around the liver and mesentery. In males the process spreads to the scrotum through the still open processus vaginalis.
Calcifications can be punctate, linear or clumping
Another outcome may be meconium pseudocyst (14% of cases), or bowel dilatation (27%)
Ascites is common (54%) and aften has internal echoes.
|Fetal ascites|| Generalized is associated with hydrops, metabolic storage diseases (Gauder's, Walman's etc)|
Local ascites is associated with GU issues (urine asictes is common), obstruction (urethrocesicular junction is most common), nephrotic syndrome, ovarian cyst with torsion, intestinal (common) meconium peritonitis, volvulus, atresia, hepatic (hepatitis with fibrosis, biliary atresia)
|Hyperechoic bowel||Can be normal if no dilated loops are seen. Then hyperechoic lumen is the only issue|
Can be secondary to wall interfaces - usually with a high frequency transmitter - try a lowe frequency one
Often pathologyic if there is mass effect on adhacent organs, and it is seen in multiple planes and frequencies, especially if it is more echogenic than adjacent bone.
In that case there in increased risk of CF, CMV, chromosomal abnormality growth retardation and perinatal death
Resoltion of echogenicity is not a sign that the bowel was normal afterall.
If detected, evaluate the whole fetus and follow-up closely
|Abdominal wall defects|| Omphalocele,|
Pentalogy of Cantrell
All distupt the anterior wall skin resulting in increased AFP level
|Omphalocele||The most common of the 4 anterior abdominal wall defects (5-10% are from Beckwith-Wideman disease)|
The defect is central. The abdominal contents are herniated into the base of the umbilicus with thin amnioperitoneal membrane
The cord inserts into anterior part of the defect or to the side.
There are 2 subtypes:
Large: contains the liver, bowel, stomach. Due to priamry failure of abdominal wall closure. The cord inserts to the side of the defect
Small: contains only bowel, due to persistance of primitive body stalk. The cord inserts midline. Look for Warton's jelly cyst at cord insertion. Differential includes umbilical hernia, hemangioma.
Heart or bladder outside the body in defect worsent prognosis
There increased risk of chromosomal abnormality (12%) - more common with small defects, Structural abnormality (75%) - more common with large defect., cardiac (30-50%), GI, GU
|Gastroschisis||Is less common than omphalocele.|
Typically less than 4 cm and goes through all layers of the wall.
Is paraumbilical, typically in the right lower quadrant.
The bowel loops float freely. The small bowel ALWAYS protrudes, large bowel less often.
The stomach or GU parts protruding is rare.
The liver definitely should not be protruding
If the bowel perforates, meconium peritonitis can ensue
Polyhydramnios is infrequent
|Cystic abdominal mass|| Rare.|
If in the lower abdomen, can represents obstructed uterus or vagina or ovarian cyst, mesenteric or duplication cyst or urachal cyst
If in the right upper quadrant can represents a liver or choledocal cyst. In the LUQ can represent spleen pathology
|Extopic kidneys|| Are usually low in the abdomen or even pelvis|
Ratio of kidney circumference is stable throughout end and 3rd trimesters. Normal is about 0.27 to 0.3
The pelvis is allowed to be up to 4 mm at 33 weeks, and upt to 7 mm after 33 weeks
|Fetal bladder||If not seen or always less than 1 cm diameter, continue sequential scans q 15 minutes to 1 hour. If still not seen, renal function is likely impaired|
|Oligohydramnios causes|| 2nd trimester|
bilateral renal abnormalities (severe)
Obstruction at bladder below (severe)
Spontaneoud rupture of membranes (mild to severe)
2nd or 3rd
Abdominal pregnancy (variable)
|Renal agenesis||Most common cause of sever bilateral renal dysfuction|
There is marked 2nd trimester oligohydramnios
The bladder is not seen or very small (<1 cm) and unchanging on sequential scans to 1 hour.
If seen and unchanging, likely contains mucus or residual urine (if kidneys inially worked then became nonfunctional)
This is ALWAYS lethal secondary to mulmonary hypoplasia from oligohydramnios.
The adrenal can move down into the empty renal fossae which can lead to false negatives
|Infantile PCKD||Actually is a tubular ectaisa|
The kidneys are enlarged and hyperechoic. Function decreases progressively. Usually still normal in the 2nd trimester with normal amniotic fluid.
Delat in oligohydramnios onset can allow the lungs to develop
The adult form can rarely be seen in nutero. The cysts can be seen if large enough, or the whole lesion can look solid/hyperechoic
Look at the hands if hyperechoic kidneys are seen.
Meckel gruber sundrome consists hyperechoic kidneys, encephalocele ad microcephaly and polydactily
Prognostic factors: If the kidney is more echoic than liver and there are cysts, dysplasia has already occured, but Absence of these signs does not imply normality.
Prune belly appearance may be present secondary to overdistended bladder (bad)
Primary prune belly sundrome is called eagle-barett syndrome, also bad prognostic factor.
|Unilateral renal anomalies|| more common tha bilateral|
usually MCDK or UPJ obstruction
As long as 1 kidney is normal, amnio volume is normal and lungs are still normal.
|Intratesticular varicocele||Basically the same condition as extratesticular, but inside the testicular parenchyma. This is rare.|
Oddly enough, the two are only associated about 11% of the time. Is bilateral in about 40% of cases.
Also, unlike extratesticular, there is near equal ocurence on right and left.
Pain is most common presentation.
Look for internal flow to differentiate from dilated rete testes
|MCDK||Seen as enlarge paraspinal structure with multiple non-communicating cysts of variable sizes with "cluster of grapes" appearance|
Normal kidney is not seen. There is hyperechoic intervening soft tissues between cysts. The ureters are atretic or not seen.
The affected kidney can be stable in size over time or can enlarge in utero.
In 20% of of cases MCDK is associated with abnormality of the contralateral side (UPJ obstruction, cysts, etc. If it is MCDK, then lethal, as then there is no normal kidney)
|UPJ obstruction|| There id dilation of the renal pelvis and calices with "Glove" appearance of true hydronephrosis.|
The uereter is normal below the level of obstruction
|Megacystis microcolon hypoperistalsis intestinalis||Combination of polyhydramnios, large bladder and enlarge ureters, small colon.|
|Adrenal glands prenatally|| Are about half the size of the neonatal kidneys.|
Usually not well defined til the 3rd trimester
Similar echogenicity to normal kidney with a hypoechoic cortex and hyperechoic medulla.
|Achondrogenesis|| Often called lionine or cherub-like facies-with very forechortened limbs.|
The long bones have nor echogenicity on US.
The axial bones are very hypoechoic with narrow, bell-shaped chest, short ribs and decreased size of spinal canal
|Thanatophoric dysplasia|| The ribs have normal birghtness on US, but the whole rib can be seen in a single plane (single image) because they are straightened and short.|
The skull has a characteristic cloverleaf shape
|Placenta on US||Seen as early as 7-8 weeks and always by 12 weeks|
The chrioamnionic membrane is seen as a bright reflector on the placental surface if perpendicular to the beam.
Thicness decreases overall with age, but the center should always be over 2 cm
Attachment at the uterus wall is to basilar myometrial layer is seen as a hypoechoic band
Serosal and juxtauterine veins are seen at the margins and lateral to the uterus.
Grade 0 placenta - has uniform echogenicity
Grade 1 - has small speckled calcifications and is seen over 30 weeks gestation
Grade 2 - similar to 1 but larger calcs and along the basilar plate, seen over 32 weeks
Grade 3 - similar to 2 but even more/thicker calcifications separating the placenta into cotyledons. Seen over 34 weeks. Can have significatn shadowing.
Up to 40$ of placentas never go beyond grade 0 or 1. 45% never go past 2. Only 15 % reach grade 3.
If calcifications are present to early, can mean dysmaturity, or associtated with growth restriction.
|Trophotropism||Is placental remodelind secondary to poor vascularity such as near scarring, large fibroids etc.|
1 - placental can shift relative to the cord insertion resulting in eccentric cord, even vilamentous cord insertion
2 - Placental can end up in unusual shape, bilobar or even succenturiate
3 - The shift can be good, resulting in resolved placenta previa
|Cord abnormalities|| Included Wharton's jelly cyst, allantoic cyst, urachal remnants|
The most common vascular cord mass is a hemangioma, which has uniform, low-level echoes and looks similar to omphalocele (causing false positive when it is close to the abdominal wall)
|Placental bleed||The most common sites are |
subchrionic and retroplacental
Subchorionic is at the margin of the placenta
Between chorioamnionic and uterine wall
Elevated the membrane from the wall
Presents with vaginal bleed
Can be asymptomatic
Outcome is usually normal
Can be a small focal collection or complete separation with extension into amniotic fluid.
Retroplacental is between placenta and uterine wall = placental abruption
When acute, the echo blends with the placenta
Can recur and enlarge
Presents with vaginal bleeding, pelvic pain, tenderness
Risks elevated wtih HTN, colagen vascular disease and trauma
|Placenta accreta, increta||Risks-prior surgery disrupting endometrial layer (cesarian)|
Pay attention to the basila-myometrial layer
Suspect if layer not seen or only seen in some areas
Also suggestive-thin/interrupted serosa, focal mass, prominent/irregular venous spaces near the disruption
Can not tell accreta, percreta and increta apart on US-except if seros in interrupted-inwhich case latter 2 are more likely
|Placental thickness||Thins with age, but center always stays over 2 cm in normal course|
-maternal vascular tissues (due to microinfarcts secondary to DM or collagen-vascular disease)
-False positive occurs with polyhydramnios because placenta is stretrched/compressed
- >4 cm at middle point
-associated wtih fetal hydrops, thalassemias, congenital infections
-gestational maternal diabetes also can cause this with macrosomic fetus but no hydrops
close f/u indicated
|Placenta previa|| Most common with combination of multiparous and prior cesarian|
Low lying = lower margin is within 2 cm of internal os
look for elevation of fetus in LUS
Stretching of cervic by fill bladder can cause a false positive
|Cervic|| Average 4 cm length +-1|
Pathologic is considered 2.5 cm or less
|Hydatidiform moles|| 85% are non-invasive, 13% invade locally, 2% metastasize|
-twins with separate sac one normal the other a mole
-incomplete mole with triploid type and residual sac and fetal tissue and possible coexisting fetus
|Theca lutein cysts|| Identified in association with molar pregnancy (sometimes)|
Can be so large they displace out of the pelvis into abdomen
The cysts can hemorrhage
|Placental infarct|| Solitary or multiple|
Most are too small to see by US
When over 1-2 cm, they are hypoechoic and simial in appearance to intervillous connection
Exact cause unknown
More common with conditionas like collagen vascular disease
If more than 50% of the placenta is effected, monitor the pregnancy for IUGR
|Placental tumors|| Chrioangioma|
Benign vascular well circumscribed solitary
when small slightly hypo, when large hetero
round or ovoid shape
can be anywhere but more often at chorionic plate bulging into amniotic fluid
internal flow with possible AV shunting = risk of hydrops secondary to high output failure
|Postpartum uterus||Involution starts immediately and complete within 6-7 weeks with most accomplished in first 3-4 weeks|
|Menopause||=beginning at 1 year after cessation of menses|
Uterus atrophies, returns to prepubertal size in 15-20 years
Body/fundus remains more prominent
Endometrial should always be <5 mm
Biopsy if any foaci of diffuse thickness over 5 mm, polyp or hyperplasia, due to risk of CA
Uterus may retain fertile appearance if there is hormonal replacement
Endometrial collection is never normal
Cervical stenosis may be due to obstructing tumor
When infected the term is pyometra
|Tamoxifen induces changes|| Endometrial thickening|
Cysts can extend to subendometrial region
US does not distinguish this from endometrial hyperplasia or carcinoma
|Polycystic ovaries|| Whole syndrome with obesity, hirsutism is called Stein-Leventhal syndrome|
There are multiple small cysts <5 mm peripherally in the ovary, which is itself rounder than normal.
The ovary may have a bright reflective capsule
Some have a normal appearance of the ovary
|Complex cyst differential|| Hemorrhage|
Duplication or mesenteric cyst
|Classic dermoid imaging|| Tip of iceberg - sound is absorbed at front edge of the mass without reflections beyong this layer|
Dermoid plug - 1 or more hyperechoic areas in the hypoechoic mass
|PID|| Perihepatic inflammation|
aka Fitz-Hugh-Curtis syndrome
|Ovarian CA||60% pts are between 40 and 60 years old, both fertile and menopoausal|
Can be silent - lack of symtpoms early on till too late
Detected usually in stage II-out of capsule, but stil in pelvis or abdomen (III)
Presents as solid or cystic mass
The more solid tissue, the higher the risk of malignancy in the mass
Vascularity also favors malignancy
No or little diastolic flow is a benign feature
Krukenberg tumor = mets from GI tract-usually solid
Cystic mets are usually from rectosigmoid CAs
|Normal fetal pleural effusion|| Between 16 and 25 weeks.|
2 ml or less
Occurs in about 71% of pregnancies
|Nonchromosomal syndromes associated with cystic hygroma|| Noonan's syndrome|
Multiple pterygioum syndrome
|Size landmarks for fetal small bowel obstruction||Small bowel loop over 7 mm diameter and over 15 mm long|
|Twin twin transfusion|| Monochorionic placenta|
Marked growth discorance >20%
Polyhydramnios in larger twin sac
Oligohydramnios in smaller twin sac
|Laryngotrahceal obstruction|| Severe but uncommon anomaly.|
Lungs uniformly enlarged and hyperechoic on US due to expansion of alveoli with fluid. The lungs are advanced in maturity. The fluid is from interstitium.
|Obligate cord|| The cord presents before the fetus. Compression of the cord by uterine contractions causes fetal heart decelerations.|
Must do C section