Repro Flashcards
The uterus
neonate
Uterus is larger than you would think for a baby (maternal / placental hormones
are still working). If you look close, the shape is a little weird with the cervix often larger than the fundus.
The uterus
prepuberty
The shape of the uterus changes - becoming more tube-like, with the cervix and uterus the same size.
The uterus
puberty
The shape o f the uterus changes again, now looking more like an adult (pear-like)
- with the fundus larger than the cervix. In puberty, the uterus starts to have a visible endometrium - with phases that vary during the cycle.
The Ovaries - Changes During Life
Just like with the uterus, infants tend to have larger ovaries (volume around 1 cc), which then
decrease and remain around or less than 1 cc until about age 6. The ovaries then gradually
increase to normal adult size as puberty approaches and occurs.
Turner Syndrome
The XO kids. Besides often having aortic coarctations, and
horseshoe kidneys they will have a pre-puberty uterus and streaky ovaries.
Embryology
The quick and dirty of it is that the mullerian ducts make the uterus and upper 2/3 of the vagina.
The urogenital sinus grows up to meet the mullerian ducts and makes the bottom 1/3 o f the vagina.
Wolffian ducts are the boy parts, and
should regress completely in girls.
Mullerian Ducts
Uterus
Fallopian Tubes
Upper 2/3 o f the Vagina
Wolffian ducts
Vas Deferens
Seminal Vesicles
Epididymis
Urogenital Sinus
Prostate
Lower 1/3 o f the Vagina
Embryology
step 1
Imagine that the stuff that makes the kidneys and the uterus is all the sam soup
you have two bowls of this stuff - half on the left, and half on the right
Embryology
step 2
as development occurs, this soup gets poured down the back of the belly
the upper part making the kiendy and the bottom part making hte uterus
Embryology
step 3
now the bottom two puddles of spilled/poured soup begin to fuse forming one puddle (uterus)
Embryology
step 4
but because they are just mashed together they dont have a central cavity necessary to carry a baby
so there is a clean - up operation (cleavage), and this occurs from bottom to top - like zipping up a jacket.
Embryology ways to screw up
1
You can only have soup on one side. This is a “failure to form” As you can imagine, if you don’t have the soup on one side you don’t have a kidney on that side. You also don’t have half o f your uterus. This is why a unilateral absent kidney is associated with Unicomuate Uterus (+/- rudimentary horn).
Embryology ways to screw up
2
As the soup gets poured down it can fail to fuse completely. This can be on the
spectrum o f mostly not fused - basically separate (Uterus Didelphys) or mostly fused
except the top part - so it looks like a heart (Bicomuate). Because the Bicomuate and
Didelphys are related pathologies - they both get vaginal septa (Didelphys more often
than Bicomuate - easily remembered because it’s a more severe fusion anomaly).
Embryology ways to screw up
3
The clean up operation can be done sloppy (“failure to cleave”). The classic example
of this is a “Septate uterus,” where a septum remains between the two uterine cavities.
Mullerian Agenesis
(Mayer-Rokitansky-Kuster-Hauser
syndrome): Has three features: (1) vaginal atresia, (2) absent or
rudimentary uterus (unicomuate or bicomuate) and (3) normal
ovaries. The key piece of trivia is that the kidneys have issues
(agenesis, ectopia) in about half the cases.
Unicornuate Uterus
4 variants
unicornuate +Communicating Cavitary Rudimentary Horn
U nicornuate + Non Communicating
Cavitary Horn
Unicornuate + Noncavitary Rudimentary Horn
Isolated unicornuate. Most Common Subtype (35%)
Unicornuate Uterus
overview
If you see a unicomuate uterus the classic teaching is to look for a rudimentary horn. The reason is the
rudimentary horns can have endometrium - and if present can cause lots of phantom female belly pain
problems (dysmenorrhea, hematometra, hematosalpinx, etc…, etc…, so on a so forth). Endometrial tissue
in a rudimentary hom (communicating or not) - increases the risk of miscarriage. An additional problem
could be a pregnancy in the rudimentary hom - in both the communicating and noncommunicating typesalthough
especially bad in the non-communicating sub-type because it nearly always results in
rudimentary hom rupture (life-threatening bleeding).
Renal agenesis contralateral to the main uterine hom (ipsilateral to the rudimentary horn) is the most
common abnonnality.
Uterus Didelphys
This is a complete uterine duplication (two cervices, two uteri, and two upper 1/3 vagina).
A vaginal septum is present 75% of the time. If the patient does not have vaginal obstruction this is usually asymptomatic.
Bicornuate uterus
This comes in two flavors (one cervix “unicollis”, or two cervix “bicollis”). There will be separation of the uterus by a deep myometrial cleft - makes it look “heart shaped”. Vaginal septum is seen around 25% of the time (less than didelphys). Although they can have an increased risk of fetal loss, it’s much less of an issue compared to Septate.
Fertility isn’t as much of a “size thing” as it is a blood supply thing. Remember you can have 8 babies in your belly at once and have them live… live long enough to take part in your reality show.
T-shaped uterus
This is the DES related anomaly. It is historical trivia, and therefore extremely high yield for the “exam of the future.” DES was a synthetic estrogen given to prevent miscarriage in the 1940s. The daughters of patients who took this
dmg ended up with vaginal clear cell carcinoma, and uterine anomalies
classically “T-Shaped.”
Septate uterus
This one has two endometrial canals separated
by a fibrous (or muscular) septum. Fibrous vs Muscular can
be determined with MRI and this distinction changes surgical
management (different approaches). There is an increased risk
o f infertility and recurrent spontaneous abortion. The septum
has a shitty blood supply, and if there is implantation on it - it
will fail early. They can resect the septum - which improves
outcomes.
This is the most common Mullerian duct anomaly associated
with miscarriage. This is improved with resection o f the
septum.
A rc u a te U te ru s
Mild smooth concavity o f the uterine
fundus (instead o f normal straight or convex) This is not really
a malformation, but more o f a normal variant. It is NOT
associated with infertility or obstetric complications.
Bicornuate quick
• “H e a rt S h a p e d ’’ - Fundal co n to u r is less than 5 mm above the tuba l ostia
• No s ig n ifica n t infertility issues
• Resection of the “s e p tum ” results in
poo r o u tcom e s
Septate quick
- Fundal co n to u r is Normal; more than 5 mm abo ve the tubal ostia
- L e g it infertility issues - impla ntation fails on the se ptum (it’s a b lo od s u p p ly th in g )
- Resection of the septum can help
Hysterosalpingogram (HSG)
overview
If you haven’t seen (or done one) before - this is a procedure that involves cannulation
of the cervix and injecting contrast under fluoro to evaluate the cavity of the uterus.
Hysterosalpingogram (HSG)
trivia
’ HSGs are performed on days 7-10 of menstrual cycle, (after menstrual bleeding complete - i.e. “off the rag”)
“ Contraindications: infection (PID), active bleeding (“rag week’’), pregnancy, and contrast allergy.
■ Bicornuate vs Septate is tough on HSG - you need MRI or 3D Ultrasound to evaluate the outer fundal contour.
Cycle days
0-7 “Rag Week,” 7-14 Proliferative, 14-28 Secretory
*Day 14 Ovulation
Salpingitis Isthmica Nodosa (SIN)
This is a nodular scarring o f the fallopian tubes that
produces an Aunt Minnie Appearance. As trivia, it
usually involves the proximal 2/3 o f the tube. This is
of unknown etiology, but likely post inflammatory /
infectious (i.e. being a woman of questionable moral
standard / “free spirit”). It’s strongly associated with
infertility and ectopic pregnancy and that is likely
the question.
Salpingitis Isthmica Nodosa (SIN)
aunt minnie
Nodular diverticula of the
fallopian tubes
No dominant channel
Uterine AVM
These can be congenital or acquired, with acquired types being way more
common. They can be serious business and you can totally bleed to death from them. The typical ways to acquire them include: previous dilation and curettage, therapeutic abortion, caesarean section, or just multiple pregnancies. Doppler ultrasound is going to show: serpiginous and/or tubular anechoic structures within the myometrium with high velocity color Doppler flow.
Intrauterine Adhesions (Ashermans) -
This is scarring in the uterus, that occurs secondary to injury: prior dilation and curettage, surgery, pregnancy, or infection (classic GU TB). This is typically shown on HSG, with either (a) non filling o f the uterus, or (b) multiple irregular linear filling defects (lacunar pattern), with inability to appropriately distend the endometrial canal. MRI would show a bunch of T2 dark bands. Clinically, this results in infertility.
Endometritis
This is in the spectrum o f P1D. You often see it 2-5 days after delivery,
especially in women with prolonged labor or premature rupture. You are going to have fluid and a thickened endometrial cavity. You can have gas in the cavity (not specific in a postpartum women). It can progress to pyometrium, which is when you have expansion with pus.
Pelvic Floor
overview
Getting old and having a bunch o f kids can sometimes make stuff hang out o f your vagina and cause you to
pee your pants (when you don’t actually want to pee your pants). It is important to make that distinction
between “prolapse” (stuff hanging out o f your vagina), and “relaxation” (peeing and/or pooping your pants
when you sneeze). Both are b a d … although one is worse — I ’ll let you decide which one that is.
Pelvic Floor
anatomy
This anatomy is complicated - buncha facial bands “ligaments” muscles etc… created a
“sling” which keeps all this stuff from falling out the bottom. The best way to think about the pelvic sling o f a
female is to group it into 3 functional compartments: Anterior compartment (bladder and urethra), Middle
compartment (vagina, cervix, uterus, and adnexa), and Posterior compartment (anus and rectum). This anatomy
is incredibly complex - but a few o f these vocab terms could make easy questions:
Pelvic Floor
endopelvic fascia
Buncha ligaments / fascia (pubocervical fascia, rectovaginal fascia, cardinal ligaments,
etc..) most o f which have vaginal or cervix in the name. Main support for the anterior & middle compartments.
Pelvic Floor
levator ani
This is the main muscular component o f the pelvic floor composed o f the puborectalis,
pubococcygeus, and iliococcygeus. This muscle groups constant contraction maintains the pelvic floor height.
Pelvic Floor Relaxation
Pelvic floor relaxation has two components (pelvic floor descent and widening) that can be graded during maximal strain on sag MR1: • Hiatal enlargement (H line) — less than 6cm - measurement o f widening • Pelvic floor descent (M line) - less than 2cm - measurement o f descent Wider H or longer M = Worse. Organs hanging out = worse.
Pelvic Floor
MRI protocol
Steady State - T2 - 3 planes Dynamic State - Rapid T2 with Fat Sat, Sag Plane Only —performed during Valsalva, Kegel, and/or taking a shit (seriously)
Pelvic Floor
PCL
(pubococcygeal line) = drawn from
inferior margin o f the symphysis pubis to
the junction between the first and second
coccygeal elements.
Pelvic Floor
H line
drawn from the inferior margin
o f the symphysis pubis to the posterior
aspect o f the puborectalis muscle sling.
Pelvic Floor
m line
shortest distance between the
posterior aspect o f the puborectalis
muscle sling and the PCL
Pelvic Floor
Axial image through the Ischioanal space
(Triangular o f fat lateral and caudally to the
levator ani - could show a loss o f the normal “H shaped” vagina or direct defects /
asymmetric thinning in the muscular sling. Having said that - for the purpose o f multiple
choice - this anatomy is usually demonstrating an anal fistula in the setting o f Crohns
Pelvic floor
urogenital diaphragm
This is the most caudal or superficial musculofascial structure. It does not have a marketable sex toy name (unlike Levator Ani). This thing usually finds it way into multiple choice exams as
the anatomic landmark used in the classification o f urethral injury - as discussed in the GU chapter.
Cystocele
overview
Bladder Descent > 1 cm
below the pubococcygeal line.
Cystocele
urethral hypermobility
what you say if the urethra is rotated horizontally. This changes the treatment f rom , retropubic urethropexy (for normal stress incontinence) to a pubovaginal sling.
Cystocele
risk factors
Squeezing a bunch of
kids out o f your vagina - can rupture
o f the pubocervical fascia
Cystocele
risk factors
Squeezing a bunch of
kids out o f your vagina - can rupture
o f the pubocervical fascia
Uterine prolapse
overview
Decent o f the cervix or posterior vaginal fornix < 1 cm above the pubococcygeal line.
A big turd can prop up the uterus - so
it is best to measure them with an
empty rectum (post defecation phase).
Uterine prolapse
risk factor
hysterectomy
Uterine prolapse
axial imag
Axial images could show the vagina
lose its normal “H” shape - hanging
low like the sleeve o f a w izard (or the
tongue o f a tired dog).
Rectocele
overview
Abnormal rectal
bulging (typically anteriorly).
Due to weakening
o f the rectovaginal fascia.
The describe them by how far
they bulge relative to the anal
canal.
Rectocele
risk factors
Vaginal surgery.
Hysterectomy, Chronic
Constipation, Being Old as
Dirt.
Fibroids (Uterine Leiomyoma)
hyaline (classic)
Most common type
T1 dark
T2 dark
Tl+C homogenous
Fibroids (Uterine Leiomyoma)
hypercellular
Densely packed smooth muscle (without much connective tissue). Respond well to embolization
T1 dark
T2 bright
Tl+C homogenous
Fibroids (Uterine Leiomyoma)
lipoleiomyoma
Rare fat containing subtype (maybe the result of degeneration!. This thing will be hvperechoic on ultrasound. Will look like a fattv uterine mass on CT. Will drop signal on fat saturation sequences.
T1 Bright (dark if fat sat)
T2 bright
Tl+C maybe rim enhancement
Fibroids (Uterine Leiomyoma)
degeneration
4 types of degeneration are generally described. What they have in common is a lack
of / paucity of enhancement (fibroids normally enhance avidly). The process of degeneration (basically
a fibroid stroke) can cause severe pain as well as fever and/or leukocytosis.
Fibroid Degeneration
Hyaline
Classic
Degeneration
Most common type. The fibroid outgrows its blood supply, and you end up getting the accumulation o f proteinaceous tissue.
T1 variable (usually dark)
T2 heterogenous ( usually dark)
Tl+C none
Fibroid Degeneration
Red
Carneous
This one occurs during pregnancy - caused by venous thrombosis. The classic imaging finding is a peripheral rim o fT l high signal.
T1 peripheral rim ov bright T1
T2 variable
Tl+C none
Fibroid Degeneration
Myxoid
Degeneration
uncommon
T1 dark
T2 bright
Tl+C minimal
Fibroid Degeneration
Cystic
Degeneration
uncommon
T1 dark
T2 bright
Tl+C none
Uterine Leiomyosarcoma
The risk o f malignant transformation to a leiomyosarcoma is super low (0.1%). These look like a fibroid, but rapidly enlarge. Areas of
necrosis are often seen.
Adenomyosis
overview
This is endometrial tissue that has migrated into the myometrium. You
see it most commonly in multiparous women of reproductive age, especially if they’ve
had a history of uterine procedures (Caesarian section, dilatation and curettage).
Adenomyosis
types
Although there are several types, adenomyosis is usually generalized, favoring large portions
of the uterus (especially the posterior wall), but sparing the cervix. It classically causes
marked enlargement o f the uterus, with preservation o f the overall contour.
Adenomyosis
imaging
They can show it with Ultrasound or MRI.
Ultrasound is less specific with findings
including a heterogeneous uterus
(hyperechoic adenomyosis, with
hypoechoic muscular hypertrophy), or just enlargement of the posterior wall. MRI is the way better test with the most classic feature being thickening of the junctional zone of the uterus to more than 12 mm (normal is < 5 mm). The thickening can be
either focal or diffuse. Additionally, the
findings o f small high T2 signal regions
corresponding to regions o f cystic change is
a classic finding.
Adenomyosis of the Uterus
T2 Bright Cystic Foci and thick junctional zone
Adenomyosis of the Uterus
T2 Bright Cystic Foci and thick junctional zone
Thick Endometrium
overview
Remember the stripe is measured without including any fluid in the canal. Focal or
generalized thickening in post menopausal women greater than 5mm should get sampled.
Premenopausal endometriums can get very thick - up to 20mm can be normal.
Thick Endometrium
trivia
• Estrogen secreting tumors - Granulosa Cell
tumors o f the ovary will thicken the
endometrium.
• Hereditary Non-Polyposis Colon Cancer
(HNPCC) - have a 30-50x increased risk of
endometrial cancer
Postmenopausal Bleeding:
Is it from atrophy or cancer?
•Endometrium less than 5 mm =
Probably Atrophy
•Endometrium > 4-5 mm = Maybe
cancer and gets a biopsy
Tamoxifen Changes
This is a SERM (acts like estrogen in the pelvis, blocks the estrogen effects on the breast). It’s used for breast cancer, but increases the risk of endometrial cancer. It will cause subendometrial cysts, and the development of endometrial polyps (30%). Normally, post menopausal endometrial tissue shouldn’t be
thicker than 4mm, but on Tamoxifen the endometrium is often thick (some papers say the mean is 12 mm at 5 years). When do you biopsy? Clear guidelines on this are illusive (if forced to guess I’d pick 8 or 10 mm). The only thing that seems consistent is that routine
screening is NOT advised. If you are wondering if a polyp is hiding you can get a sonohysterogram (ultrasound after instillation o f saline).
Endometrial Fluid
In premenopausal women this is a common finding. In postmenopausal women it means either cervical stenosis or an obstructing mass (usually
cervical stenosis).
Endometrial Fluid
In premenopausal women this is a common finding. In postmenopausal women it means either cervical stenosis or an obstructing mass (usually
cervical stenosis).
Endometrial Cancer
overview
Basically all uterine cancers are adenocarcinoma (90%+). The only possible exception for the purpose o f multiple choice would be the rare “leiomyosarcoma” - which looks like a giant fucking fibroid.
Endometrial Cancer
typical scenario
A postmenopausal patient (60s) with bleeding.
Endometrial Cancer
work up
First step is going to be an ultrasound. If the endometrium is too thick (most
people say 4- 5mm) then it gets a biopsy. Almost always this will be stage 1 disease, and no further imaging will be done. If there is concern that it’s more than stage 1 - that is
when you would get MRI (CT is shit for the uterus and would never be the right answer).
• First Step Postmenopausal Bleeder = Ultrasound
• Too Thick ? = Biopsy
• Extent of Disease = MRI
Endometrial Cancer
appearance on MRI
- T1 Iso
- T2 Mildly Hyper
- Tl+C Homogenous, but less enhancement compared to adjacent myometrium ( it’s dark).
- DWI Will show restricted dijfusion. This sequence is good fo r “Drop mets ” into the vagina, and fo r lymph node detection.
Endometrial Cancer
critical stage
• Stage 2 disease is defined as cervical stroma invasion. This is supposedly high risk for
lymph node mets.
• The diagnostic key is the post contrast imaging (obtained 2-3 mins after injection). If
the cervical mucosa enhances normally, you have excluded stromal invasion.
• Stage 2 is probably going to change management by adding pre-op radiation to the
cervix, plus a change from TAH to radical hysterectomy (obviously this varies from
center to center).
Endometrial Cancer
stage 1 imaging
T1+C: Normal Dark Cervical Stroma (star).
Enhancement of the Cervical Mucosa
(arrows) Excludes Invasion.
Endometrial Cancer
stage 2 imaging
T1+C: Tumor Invasion o f the Cervix
Endometrial Cancer
other possible trivia
• Moving from stage 1A (<50% myometrium) to stage 1B (>50% o f the myometrium)
also increases the risk o f lymph node disease.
• Some sites will do lymph node sample at stage 1 A, and radical lymph node dissection at stage IB.
Cervical Cancer
overview
It’s usually squamous cell, related to HPV (like 90%). The big thing to know is parametrial invasion (stage lib). Stage Ila or below is treated with surgery. Once you have parametrial invasion (stage lib), or involvement o f the lower 1/3 o f the vagina it’s gonna get chemo/ radiation. In other words, management changes so that is the most likely test question.
Cervical Cancer
stage IIA
Spread beyond the cervix, but NO parametrial invasion
Surgery
Cervical Cancer
Stage IIB
Parametrial involvement but NOT extension to pelvic side wall.
Chemo/ Radiation
Cervical Cancer
what is the parametrium
The p aram etrium is a fib ro u s b an d that separates the supravaginal cervix from the bladder. It e x te n d s between the layers of the bro ad ligament.
Cervical Cancer
why is the parametrium important
The uterine artery runs inside the parametrium, hence the need for chemo - o n ce in va de d .
Cervical Cancer
how do you tell if the parametrium is invaded
Normally the ce rv ix has a T2 d a rk ring. That thing should be intact. If the tum o r goes throug h th a t thing, you g otta call it invaded.
Solid Vaginal Masses
An uninvited solid vaginal mass is usually a bad thing. It can be secondary (cervical or uterine carcinoma protruding into the vagina), or primary such as a clear cell adenocarcinoma or rhabdomyosarcoma.
leiomyoma
squamos cell carcinoma
clear cell adenocarcinoma
vaginal rhabdomyosarcoma
Solid Vaginal Masses
Leiomyoma
Rare in the vagina, but can occur (most commonly in the anterior wall).
Solid Vaginal Masses
Squamous Cell Carcinoma
The most common cancer of the vagina (85%). This is associated with HPV. This is just like the cervix.
Solid Vaginal Masses
Clear Cell Adenocarcinoma
This is the zebra cancer seen in women whose mothers took DES (a synthetic estrogen thought to prevent miscarriage). That plus “T-Shaped Uterus” is probably all you need to know.
Solid Vaginal Masses
Vaginal Rhabdomyosarcoma
This is the most common tumor o f the vagina in children. There is a bimodal age distribution in ages (2-6, and 14-18). They usually come off the anterior wall near the cervix. It can occur in the uterus, but typically invades it secondarily. Think about this when you see a solid T2 bright enhancing mass in the vagina / lower uterus in a child.
Solid Vaginal Masses
mets trivia
- A met to the vagina in the anterior wall upper 1/3 is “always ” (90%) upper genital tract.
- A met to the vagina in the posterior wall tower 1/3 is “always ” (90%) from the Gl tract.
Cystic Vaginal I Cervical Masses
Nabothian Cysts
These are usually on the cervix and you see them all the time. They are
the result o f inflammation causing epithelium plugging o f mucous glands.
Cystic Vaginal I Cervical Masses
Gartner Ducts Cysts
These are the result o f incomplete regression of the Wolffian ducts.
They are classically located along the anterior lateral wall of the upper vagina. If they are located at the level o f the urethra, that can cause mass effect on the urethra (and symptoms).
Cystic Vaginal I Cervical Masses
Bartholin Cysts
These are the result o f obstruction o f the Bartholin glands (mucinsecreting
glands from the urogenital sinus). They are found below the pubic symphysis
(helps distinguish them from Gartner duct).
Cystic Vaginal I Cervical Masses
Skene Gland Cysts
Cysts in these periurethral glands, can cause recurrent UTIs and urethral obstruction.
Gartner duct cyst quick
anterior lateral upper vagina
Bartholin gland cyst quick
— “Ba rth o lin is B e low ” the p u b ic s ymphysis
— “B a rth o lin is n e a r the Butthole.
O V A R Y / A D N E X A
ovulation
Follicles seen during the early menstrual cycle are typically small (< 5 mm in diameter). By day 10 of the cycle, there is usually one follicle that has emerged as the dominant follicle. By mid cycle, this dominant follicle has gotten pretty big (around 20 mm). The size isn’t surprising because it contains a mature ovum. The LH surge causes the dominant follicle to
rupture, releasing the egg. The follicle then regresses in size, forming a Corpus Luteum. A small amount of fluid can be seen in the cul-de-sac. Occasionally, a
follicle bleeds and re-expands (hemorrhagic cyst) - more on this later.
O V A R Y / A D N E X A
ovulation quick
LH durring faollicular phase with dominant follicle right before ovulation then LH surge with ovulation then luteal phase with corpus luteum
O V A R Y / A D N E X A
meaningless vocab premenopausal ovarian cyst
< 1 cm = Follicle
1-2 cm = Dominant Follicle
> 3 cm = Cyst
Cumulus Oophorus
This is a piece of anatomy trivia. It is a collection of
cells in a mature dominant follicle that protrudes into the
follicular cavity, and signals imminent ovulation (its
absence means nothing).
Fertility Meds
Medications such as a Clomiphene Citrate (Clomid), force the maturation of multiple
bilateral ovarian cysts. It is not uncommon for the ovaries of women taking this drug
to have multiple follicles measuring more than 20 mm in diameter by mid cycle.
Theca Lutein Cysts
this is a type of functional
cyst (more on that below), related to overstimulation
from b-HCG. What you see are large cysts (~ 2-3 cm)
and the ovary has a typical multilocular cystic “spokewheel”
appearance.
Theca Lutein Cysts
think about 3 things
- Multifetal pregnancy,
- Gestational trophoblastic disease (moles),
- Ovarian Hyperstimulation syndrome.
Ovarian Hyperstimulation Syndrome
This is a complication associated with fertility therapy (occurs in like 5%). They will show you the ovaries with theca lutein cysts, then ascites,
and pleural effusions. They may also have pericardial effusions. Complications include increased
risk for ovarian torsion (big ovaries) and hypovolemic shock.
Paraovarian (Paratubal) Cyst
Cyst that is in the adnexa but not within the ovary. Instead
these things are located adjacent to the ovary or tube. If the cyst is simple (not septated or nodular) and
clearly not ovarian they will not need followup — is doesn’t matter how big it is, as they have incredibly
low rate of malignancy.
TLDR
Simple paraovarian cysts do not require follow up.
TLDR
Simple paraovarian cysts do not require follow up.
Premenstrual ovaries
- The ovaries o f a pediatric patient stay small until around age 8-9.
- Ovaries may contain small follicles.
premenopausal ovaries
- A piece o f trivia; premenopausal ovaries may be HOT on PET (depending on the menstrual cycle).
- This is why you do a PET in the first week o f the menstrual cycle.
postmenopausal ovaries ( > one year after menses stops):
- Considered abnormal if it exceeds the upper limit of normal, or is twice the size of the other ovary (even if no mass is present).
- Small cysts (< 3 cm) are seen in around 20% o f post menopausal women.
- In general, postmenopausal ovaries are atrophic, lack follicles, and can be difficult to find with ultrasound.
- The ovarian volume will decrease from around 8cc at age 40, to around 1 cc at age 70.
- The maximum ovarian volume in a post menopausal woman is 6 ml.
- Unlike premenopausal ovaries, post menopausal ovaries should NOT be hot on PET.
Ovarian cyst
If the cyst is simple, regardless o f age it’s almost
certainly benign.
What if they don’t tell you if the patient is pre or post menopausal ? You can use 50 years old as a cut off. Under 50 Pre, 50 & up Post.
Incidental Simple Appearing Ovarian Cyst -Shown on CT
PreMenopausal:< 3 cm = Call it Normal Follicle
PreMenopausal: > 3 cm = Get an US
PostMenopausal: < 1cm = Call it Normal Cyst
PostMenopausal: > 1cm = Get an US
Incidental Simple Appearing Ovarian Cyst
-Shown on US
PrcMenopausal:< 7 cm = No Follow Up
PreMenopausal: > 7 cm = Follow Up (3 months)
PostMenopausal: < 5 cm = No Follow Up
PostMenopausal: > 5 cm = Follow Up (3 months)
Ovarian cyst that is not simple
Cyst is not simple (irregular septations, papillary proiections. or solid elements) = GYN consult.
Sinister six ovraian masses
In most clinical practices, the overwhelming majority o f ovarian masses are benign (don't worry, I’ll talk about cancer, too). Physiologic and functioning follicles Corpora lutea Hemorrhagic cysts Endometriomas Benign cystic teratomas (dermoids) Polycystic ovaries
Functioning Ovarian Cysts
Functioning cysts (follicles) are affected by the menstrual
cycle (as I detailed eloquently above). These cysts are benign and usually 25 mm or less in
diameter. They will usually change / disappear in 6 weeks. If a cyst persists and either does not
change or increases in size, it is considered a nonfunctioning cyst (not under hormonal control).
Simple cysts that are > 7 cm in size may need further evaluation with MR (or surgical
evaluation). Just because it’s hard to evaluate them completely on US when they are that big,
and you risk torsion with a cyst that size.
Corpus Luteum
The normal corpus luteum arises from a dominant follicle (as I detailed
eloquently above). These things can be large (up to 5-6 cm) with a variable appearance (solid
hypoechoic, anechoic, thin-walled, thick-walled, cyst with debris). The most common
appearance is solid and hypoechoic with a “ring of fire” (intense peripheral blood flow).
THIS v.v THAT: Corpus Luteum VS Ectopic Pregnancy
They both can have that “ring of fire” appearance, but please don’t be an idiot about this. Most ectopic pregnancies occur in the tube (the corpus luteum is an ovarian structure). If you are really lucky, a “hint” is that the corpus luteum should move with the ovary, where an ectopic will move separate from the ovary (you can push the ectopic away from it). Also, the tubal ring of an ectopic pregnancy is usually more echogenic when compared to the ovarian parenchyma. Whereas, the wall of the corpus luteum is usually less echogenic. A specific (but not sensitive) finding in ectopic pregnancy is a RI of <0.4 or >0.7.
Ectopic quick
RI <0.4, or >0.7
Thick echogenic rim
Ring of fire
moves separate from the ovary
Corpus luteum quick
RI 0 .4 -0 .7
thin echogenic rim
ring of fire
moves with the ovary
Endometrioma
epidemiology
This targets young women during their reproductive years and can cause chronic pelvic pain
associated with menstruation. The traditional clinical history of endometriosis is the triad of
infertility, dysmenorrhea, and dyspareunia.
Endometrioma
classic appearance
The classic appearance is rounded mass with homogeneous low level internal echoes and
increased through transmission (seen in 95% of cases). Fluid-fluid levels and internal septations
can also be seen. It can look a lot like a hemorrhagic cyst (sometimes).
Endometrioma
imaging findings
As a general rule, the more unusual or varied the
echogenicity and the more ovoid or irregular the shape, the
more likely the mass is an endometrioma. Additionally,
and of more practical value, they are not going to change
on follow up (hemorrhagic cysts are). In about 30% of
cases you can get small echogenic foci adhering to the
walls (this helps make the endometrioma diagnosis more
likely). Obviously, you want to differentiate this from a
true wall nodule.
Endometriosis
complications
The complications of endometriosis (bowel obstruction, infertility, etc…) are due to a fibrotic
reaction associated with the implant. The most common location for solid endometriosis is the
uterosacral ligaments.
Endometrioma
becoming cancer
About 1% of endometriomas undergo malignant transformation (usually endometrioid or clear cell carcinoma). How do you tell which one is which??? Malignancy is very rare in endometriomas smaller than 6 cm. They usually have to be bigger than 9 cm. Additionally, the majority of women with carcinoma in an endometrioma are older than 45 years. So risk factors for turning into cancer: (a) older than 45, (b) bigger than 6-9 cm.
Endometrioma
pregnancy trivia
There is a thing called a “decidualized
endometrioma. ” This is a vocab word used to describe a
solid nodule with blood flow in an endometrioma of a
pregnant girl. Obviously this is still gonna get followed up
- but is a mimic of malignancy. The thing never to forget
is that if the patient is NOT pregnant and you see a solid
nodule with blood flow - that is malignant degeneration -
period - no hesitation, next question.
Endometrioma
on MRI
Will be T1 bright (from the blood). Fat saturation will not suppress the signal (showing you it’s not a teratoma). Will be T2 dark! (from
iron in the endometrioma). The shading sign is a buzzword
for endometriomas on MR imaging. On T2 you should
look for “shading.” The shading sign describes T2
shortening (getting dark) of a lesion that is T1 bright.
Endometrioma
What is the most sensitive imaging feature on MR1 for the diagnosis of malignancy in an endometrioma ?
an enhancing mural nodule
Endometrioma mri findings quick
T1 bright
T2 shaded
Hemorrhagic Cysts
overview
As mentioned on prior pages, sometimes a ruptured follicle bleeds internally and reexpands.
The result is a homogenous mass with enhanced through transmission (tumor
w o n ’t do that) with a very similar look to an endometrioma. A lacy “fishnet appearance”
is sometimes seen and is considered classic. Doppler flow will be absent. The traditional
way to tell the difference between a hemorrhagic cyst vs endometrioma, is that the
hemorrhagic cyst will go away in 1-2 menstrual cycles (so repeat in 6-12 weeks).
Hemorrhagic Cysts
MRI
Will be T1 bright (from the blood). Fat saturation will not
suppress the signal (showing you it’s not a teratoma). The lesion should NOT enhance.
Hemorrhagic Cysts
old ladies
Postmenopausal women may occasionally ovulate, so
you don’t necessarily need to freak out (follow up in 6-12 weeks). Now, late
postmenopausal women should NEVER have a hemorrhagic cyst and if you are shown something that looks like a hemorrhagic cyst in a 70 year old - it’s cancer till proven otherwise.
THIS vs THAT: E n d om e triom a vs H em o r rh a g ic C ys t
us
Endometrioma - Homogeneous with Low Level Echoes
Hemorrhagic Cyst - Lacy fishnet appearance
Dermoid
overview
These things typically occur in young women (20s-30s), and are the most common ovarian
neoplasm in patients younger than 20. The “Tip of the Iceberg Sign” is a classic buzzword and
refers to absorption of most of the US beam at the top of the mass. The typical ultrasound
appearance is that of a cystic mass, with a hyperechoic solid mural nodule, (Rokitansky nodule or
dermoid plug). Septations arc seen in about 10%.
Dermoid
MRI
Will be bright on T1
(from the fat). There will be fat
suppression (not true of hemorrhagic
cysts, and endometriomas).
Dermoid
do they ever become cancer
About l% of dermoids can undergo malignant
transformation (almost always to squamous cell CA). Again, risk factors are size (usually
larger than 10cm), and age (usually older than 50).
Dermoid
gamesmanship 1
Gross Fat containing ovarian mass on CT
Dermoid
gamesmanship 2
The Old Tooth Trick - shown on plain film, CT, or even as susceptibility (dark stuff) on MR. Remember Dermoids are basically teratomas, and teratomas grow all kinds of gross shit including teeth, hair, finger nails etc… The tooth is obviously the classic one.
Dermoid
gamesmanship 3
“Dot -dash” pattern has been described for hair within a cyst.
Rare Cancer Transformation Subtypes
Endometrioma > Clear Cell
Dermoid > Squamous
Endometrioma quick MRI
T2 mild hyperintense
Dermoid quick MRI
T1FS hypointense
Hemorrhagic cyst quick MRI
T1, T1FS, T2 hyperintense
Polycystic Ovarian Syndrome
overview
Typically an overweight girl with infertility, acne, and a pencil mustache (not a full Ron Swanson)
Polycystic Ovarian Syndrome
imaging
Ten or more peripheral simple cysts (typically small < 5 mm)
Usually Characteristic ‘string-of-pearls’ appearance.
Ovaries are typically enlarged (> 10 cc),
although in 30% of patients the ovaries have a normal volume
Ovarian Cancer
overview
Ovarian cancers often present as complex cystic and solid masses. They are typically intraovarian
(most extra-ovarian masses are benign). The role o f imaging is not to come down
hard on histology (although the exam may ask this of you), but instead to distinguish benign
from malignant and let the surgeon handle it from there.
Ovarian Cancer
think cancer if
Unilateral (or bilateral) complex cystic adnexal masses with thick ( > 3 mm)
septations, and papillary projections (nodule with blood flow).
Solid adnexal masses with variable necrosis
Ovarian Cancer
knee jerks
Multiple thin or thick septations = Call the Surgeon
Nodule with Flow = Call the Surgeon
Solid Nodules Without Flow =
o Get an MR to make sure it’s not a dermoid plug,
o If it’s not a dermoid, then call the surgeon
Mucinous O v a rian C y s tad e n o c a rc in om a
Often a large mass. They are typically multi-loculated (although septa are often thin).
Papillary projections are less common than with serous tumors. You can see low level
echos (from mucin). These dudes can get Pseudomyxoma peritonei with scalloping
along solid organs. Smoking is a known risk factor (especially for mucinous types).
THIS vs THAT: Serous vs Mucinous
Serous:
Unilocular (fewer septations)
Papillary Projections Common
Mucinous:
Multi-locular (more septations)
Papillary Projections Less Common
E n dome trio id O v a rian C an c e r:
overview
This is the second most common ovarian cancer (serous
number one, mucinous number three). These things are
bilateral about 15% o f the time.
E n dome trio id O v a rian C an c e r:
thigns to know
• 25% o f women will have concomitant endometrial cancer,
with the endometrial cancer as the primary (ovary is met).
• Endometriomas can turn into endometrioid cancer
• 15% are bilateral
Gamesmanship:
Ovarian Mass +
Endometrial Thickening
This is a way to show both Endometrioid CA (which often has both ovarian and endometrial CA), and Granulosa-Theca Cell Tumor (which produce estrogen - and cause endometrial hyperplasia)
B.F.M’s - for Adults
It’s useful to have a differential for a B.F.M.
(Big Fucking Mass) in an adult and a child. I
discuss the child version o f this on page 58.
For adults think about 3 main things:
(1) Ovarian Masses - Mucinous and Serous
(2) Desmoids - Remember Gardner Syndrome
(3) Sarcomas
Fibroma I Fibrothecoma
The ovarian fibroma is a benign ovarian tumor, most commonly seen in middle aged women.
The fibrothecoma / thecoma spectrum has similar histology. It’s very similar to a fibroid. On
ultrasound it’s going to be hypoechoic and solid. On MRI it’s going to be T1 and T2 dark, with
a band of T2 dark signal around the tumor on all planes. Calcifications are rare.
Meigs syndrome
This is the triad of ascites, pleural effusion, and a benign ovarian tumor
(most commonly fibroma).
Fibromatosis
This is a zebra. You have tumor-like enlargement of the
ovaries due to ovarian fibrosis. It typically hits girls around the age of 25.
It’s associated with omental fibrosis and sclerosing peritonitis. You are
going to get dark T1 and T2 signal. The buzzword for that T2 signal is
“black garland sign. ” The condition is benign, and sometimes managed
with surgical removal of the ovaries.
brenner tumor
Epithelial tumor of the ovary seen in women in their 50s-70s. It’s fibrous
and T2 dark. Unlike Fibromas, calcifications are common (80%). They are also sometimes
referred to as “Ovarian Transitional Cell Carcinoma ” for the purpose of fucking with you.
Struma Ovarii:
These things are actually a subtype of ovarian teratoma. On imaging you are looking for a
multilocular, predominantly cystic mass with an INTENSELY enhancing solid component. On
MRI - the give away is very low T2 signal in the “cystic” areas which is actually the thick
colloid. These tumors contain THYROID TISSUE, and even though it’s very rare (like 5%), I
would expect that the question stem will lead you to this diagnosis by telling you the patient is
hyperthyroid or in a thyroid storm.
Metastatic Disease to the Ovary
Around 10% of malignant ovarian tumors are mets. The primary is most commonly from colon, gastric, breast, lung, and contralateral ovary. The most common look is bilateral solidtumors.
Krukenburg Tumor
This is a metastatic tumor to the ovaries from the GI tract (usually stomach).
Ovarian Torsion
overview
Rotation of the ovarian vascular pedicle (partial or complete) can result in obstruction to venous outflow and arterial inflow. Torsion is typically associated with a cyst or tumor (anything that makes it heavy, so it flops over on itself).
Ovarian Torsion
critical point
The most constant finding in ovarian torsion is a large ovary.
Ovarian Torsion
features
Unilateral enlarged ovary (greater than 4 cm) Mass on the ovary Peripheral Cysts Free Fluid Lack of arterial or venous flow
Ovarian Torsion
the ovary is not a testicle
The ovary has a dual blood supply. Just because you have flow, does
NOT mean there isn’t a torsion. You can torse and de-torse. In other words, big ovary + pain = torsion. Clinical correlation recommended.
Hydrosalpinx
overview
There are a variety of causes, the most common is being a skank, infidel, or free spirit (PID).
Additional causes include endometriosis, tubal cancer, post hysterectomy (without salpingectomy /
oophorectomy), and tubal ligation. Rare and late complication is tubal torsion.
Hydrosalpinx
buzz 1
Thin (or thick in chronic states) elongated tubular structure in the pelvis.
Hydrosalpinx
buzz 2
The buzzword is “cogwheel appearance,” referring to the normal longitudinal folds of a
fallopian tube becoming thickened. Another buzzword is “string sign” referring to the
incomplete septae. The “waist sign” describes a tubular mass with indentations of its opposing walls
(this is suppose to help differentiate hydrosalpinx from an ovarian mass).
Pelvic Inflammatory Disease (PID)
overview
Infection or inflammation of the upper female genital tract. It’s usually secondary to the cultural
behaviors of trollops and strumpets (collectors of Gonorrhea / Chlamydia). As a hint, the question
writer could describe the patient as “sexually disreputable. ” The question could also describe the
patient as recently appearing as a guest on the Maury Show (the “Not the Father!” show — google if
unfamiliar, it could be on the exam).
Pelvic Inflammatory Disease (PID)
us findings
On ultrasound you are gonna see a Hydrosalpinx. The margin of the uterus may become ill defined
(“indefinite uterus” - is a buzzword). Later on you can end up with tubo-ovarian abscess or pelvic
abscess. You can even get bowel or urinary tract inflammatory changes.
Paraovarian Cyst
This is a congenital remnant that arises from the Wolffian duct. They are more common than you
think with some texts claiming these account for 10-20% of adnexal masses. They are classically
round or oval, simple in appearance, and do NOT distort the adjacent ovary (key finding). They
can indent the ovary and mimic an exophytic cyst, but a good sonographer can use the transducer to
separate the two structures.
Ovarian Vein Thrombophlebitis
This is seen most commonly in postpartum women, often presenting with acute pelvic pain and
fever. For whatever reason, 80% of the time it’s on the right. It’s most likely to be shown on CT
(could be ultrasound) with a tubular structure with an enhancing wall and low-attenuation thrombus
in the expected location of the ovarian vein. A dreaded sequela is pulmonary embolus.
Peritoneal Inclusion Cyst
This is an inflammatory cyst of the peritoneal cavity that occurs when adhesions envelop an ovary.
Adhesions can be thought of as diseased peritoneum. Whereas the normal peritoneum can absorb
fluid, adhesions cannot. So, you end up with normal secretions from an active ovary confined by
adhesions and resulting in an expanding pelvic mass. The classic history is patient with prior pelvic
surgery (they have to tell you that, to clue you in on the presence of adhesions), now with pain.
They could get tricky and say history of PID or endometriosis (some kind of inflammatory process to
piss off the peritoneum). In that case, it is likely they would show an ultrasound (or MR) with a
complex fluid collection occupying pelvic recesses and containing the ovary. It’s not uncommon to
have septations, loculations, and particulate matter within the contained fluid.
Peritoneal Inclusion Cyst
key features
- Lack of walls. “Passive shape” that conforms to and is defined by surrounding structures.
- Entrapment of an ovary. Ovary will be either in the collection, or at the periphery.
Peritoneal Inclusion Cyst
classic vignette
A woman of reproductive age with a history of endometriosis, pelvic surgery, and pelvic inflammatory disease. Accompanied by images (most likely ultrasound, less likely CT or MR)
or a fluid-filled mass that conforms to the shape of the pelvis and surrounds an ovary.
Gestational Trophoblastic Disease
Think about this with marked elevation of B-hCG. They will actually trend betas for tumor
activity. Apparently, elevated B-hCG makes you vomit - so hyperemesis is often part of the
given history. Other pieces of trivia is that moles are more common in ages over 40, and prior
moles makes you more likely to get another mole.
Hydatidiform Mole
overview
This is the most common form, and the benign form of the disease. There are two subtypes
Hydatidiform Mole
Complete Mole overview
(classic mole) (70%): This one involves the entire placenta. There will be no
fetus. The worthless trivia is that the karyotype is diploid. A total zebra scenario is that you
have a normal fetus, with a complete mole twin pregnancy (if you see that in the wild, write it
up). The pathogenesis is fertilization of an egg that has lost its chromosomes (46XX).
Hydatidiform Mole
Complete Mole first trimester us
Classically shows the uterus to be filled with an echogenic, solid, highly vascular mass, often described as “snowstorm” in appearance.
Hydatidiform Mole
Complete Mole second trimester us
Vesicles that make up the mole enlarge into individual cysts (2-30 mm) and produce your “bunch of grapes” appearance.
Hydatidiform Mole
Partial mole overview
(30%): This one involves only a portion of the placenta. You do have a fetus, but
it’s all jacked up (triploid in karyotype). The pathogenesis is fertilization of an ovum by two sperm (69XXY). Mercifully, it’s lethal to the fetus.
Hydatidiform Mole
partial mole us
The placenta will be enlarged, and have areas of multiple, diffuse anechoic lesions. You may see fetal parts.
Hydatidiform mole
theca lutein cyst
Remember I mentioned that Theca Lutein cysts are seen in molar pregnancies.
Theca Lutein Cyst Trivia: Most commonly bilateral and seen in the second trimester
Invasive Mole
This refers to invasion of molar tissue into the myometrium. You typically see it after the
treatment of a hydatidiform mole (about 10% of cases). US may show echogenic tissue in the
myometrium. However, MRI is way better at demonstrating muscle invasive. MRI is going to
demonstrate focal myometrial masses, dilated vessels, and areas of hemorrhage and necrosis.
Choriocarcinoma
the guacamole has gone bad
This is a very aggressive malignancy that forms only trophoblasts (no villous structure). The
typical attacking pattern of choriocarcinoma is to spread locally (into the myometrium and
parametrium) then to spread hematogenous to any site in the body. It’s very vascular and bleeds
like stink. The classic clinical scenario is serum p-hCG levels that rise in the 8 to 10 weeks
following evacuation of molar pregnancy. On ultrasound, choriocarcinoma (at any site) results in
a highly echogenic solid mass. Treatment = methotrexate.
Fractured Penis
overview
This is one of the most tragic situations that can occur in medicine.
There are several potential mechanisms of injury. Anecdotally, it seems to be most common
in older men participating in extra-marital relations with strippers named “Whisper.” There
is at least one article stating “impotence” is protective - which makes sense if you think
about the pathophysiology.
They can show it on ultrasound (look for hematoma) or MRI.
Fractured Penis
key trivia
Defined by fracture of the corpus
cavernosum and its surrounding sheath, the tunica
albuginea (black line outlining the dong bone).
Fractured Penis
cartooned t1 axial through the dong bone
Interruption of the black line (tunica albuginea) - arrow.
It’s helpful to look for hemorrhage (Tl bright) in the
corpus cavernosum (the primary stabilizing stmt of this battering ram).
Fractured Penis
stigmata
Stigmata of this injury can include a sub optimal angulation (Peyronie disease) from fibrous scar formation.
Prostate
cancer overview
Biopsy of the prostate is a terrible terrible situation, worse than anything you can
imagine in 1000 years of hell. MR1 of the prostate (instead of biopsy) is probably a little better
although many sites use an endorectal coil.. .my God this endorectal coil! You can use prostate
MRI for high risk screening (high or rising PSA with negative biopsy), or to stage (look for
extracapsular extension).
Prostate
anatomy
Anatomists like to use
“zones” to describe locations, and it actually helps with
pathology. The anterior fibromuscular gland is dark on T1 and
T2. The central and transitional zones (together called the
“centralgland”) are brighter than the anterior muscular zone,
but less bright than the peripheral zone on T2. In other words
the peripheral zone is the most T2 bright.
Prostate
adenocarcinoma zone breakdown
Peripheral Zone: 70%
Transition Zone: 20%
Central Zone: 10%
Prostate
base zones
transitional zone - inner
cetnral zone - middle
peripheral zone - outer
Prostate
midgland zones
central zone - inner
peripheral zone- outer
Prostate
apex zones
just peripheral zone
Prostate
done confuse
zones and glands
Prostate
dark stuff
central gland
where bph nodules live
Prostate
bright stuff
peripheral zone
where cancer lives
MRI finding for Prostate CA
Cance r is d a rk on T2 (background is h ig h ), restricts on
diffusion (low on ADC), and enhances early and washes out (type 3 curve - just like a breast cancer).
Prostate bone mets
bone scan
prostate cancer trivia
PSA can be useful when considering risk of bone mets. There is at least 1 paper that
says a PSA < 20 has a high predictive value in mling OUT skeletal mets. In other words,
PSA tends to be high when disease is aggressive enough to go to the bones.
prostate cncer staging
The main thing to know is stage II vs stage III, as extra capsular extension is the most important factor governing treatment.
Prostate cancer stage II
Confined by capsule (T2)
Abutment o f the capsule
without bulging
Prostate cancer stage III
Extension through capsule (T3a)
Bulging o f the capsule,
or frank extension through it
Prostate urologists
Seminal vesicles (T3b) and the nerve bundle are also right behind the prostate and can get invaded (urologists love to hear about that).
Prostate cancer
key concept
Prostate Cancer is a lot like Breast Cancer - in that it is
very common and often a “benign” entity (1 in 6 men will be diagnosed
with prostate cancer , 3% will die o f it). There are tons and tons of
elderly people with low grade prostate CA and breast cancers (DCIS)
that will never even know they have it unless somebody does a biopsy
on them… or worse performs screening on them. Which brings us to
the PSA. When family medicine doctors starting doing PSA checks on
everybody suddenly there was this enormous spike in the incidence o f
prostate cancer. Suddenly everyone has cancer (I blame the liberal media).
Prostate cancer
Clinically Significant Cancer:
Gleason Score > 7
Cancer Volume > 0.5cc
Extension through the Capsule (loss o f normal T2 signal in the seminal vesicle, bulging of the capsule / frank invasion through it, loss o f fat between prostate and rectum, neurovascular bundle asymmetry).
Prostate cancer
Who Dies of Prostate Cancer ?
There are 3 factors - Gleason Scores
8-10, Advanced Clinical Stage (mets), and PSA > 20. People with
Gleason scores less than 6, PSA < 10, and staging < 2a (less than half
the lobe) are unlikely to die o f the prostate cancer.
Prostate cancer
management
It is gonna depend a lot on who you ask. Most people will add hormone therapy around stage 2B (more than half the lobe) but it is complicated.
Prostate cancer
PSA
This is an antigen produced by the normal prostate and incorporated into the ejaculate (from the window
to the wall), for the purpose of dissolving cervical mucus e tc … It also leaks out into the blood in small amounts
in normal men and in larger amounts when the prostate is abnormal (cancer, infected, riding a bicycle, sticking
stuff up your ass that don’t belong up your ass, and benign hypertrophy). Family Medicine docs will screen
people starting at 50. Some numbers to have a vague familiarity with include: Normal < 4. Low Risk Category
< 10. High Risk Category > 20. After prostatectomy normal is zero, if it rises to 0.2 think recurrence. After
radiation anything over 2.0 is concerning for recurrence (although it’s a little more complicated than that). PSA < 20 = bone mets unlikely.
Prostate cancer
Gleason
There is a “grade” a “ score” and a “group” - you better fucking believe the distinction is fair game..
• Gleason Grade: This refers to the histological patterns in the sample “ 1” is normal, “5” is very very not
normal. 2-4 are in the middle.
• Gleason Score: This is the sum of the two most common “grades.” The more common pattern is always first.
So “A” 3+5 = 8, and “B” 5+3 = 8. “B” has more of 5 than “A” and is therefore worse off. Total scores less
than 6 aren’t usually reported.
• Gleason Group: This uses pattern scores to reflect the actual risk. This removes the confusion over one 7
being worse than another 7. For example 3+4 is grade 2, and 4+3 is grade 3. Grade is 1-5
PI-RADS
overview
Scores are calculated by using data from DWI, T 2, and Enhancement. Tumor in the Transition zone
is determined primarily from T2 (t for t). Peripheral zone is determined primarily from DWI.
PI-RADS
PZ-DWI
1-Normal
2-Linear / Wedge
3-Vague Patchy (goes to 4 with enhancement)
4-Focal < 1.5 cm
5-Focal > 1.5 cm or with extracapsular ext
PI-RADS
TZ-T2
1-Normal Nodules - full capsule
2-Atypical Nodule - no capsule (goes to 3 with coal restricted DWI)
3-Heterogenous, blurry margins (goes to 4 with restricted DWI > cm)4-Low Signal < 1,5 cm
5-Low Signal > I.5 cm or with extracapsular ext
Benign prostatic hyperplasia (BPH):
overview
Obviously this is super common, and makes
old men pee a lot. Volume o f 30cc is one definition. Most commonly involves the
transitional zone (cancer is rare in the transitional zone - 10%). The central gland enlarges
with age. The median lobe component is the one that hypertrophies and sticks up into the
bladder. It can cause outlet obstruction, bladder wall thickening (detrusor hypertrophy), and
development of bladder diverticulum.
Benign prostatic hyperplasia (BPH):
ivp buzzword
The IVP buzzword is “J shaped”, “Fishhook”, or “Hockey stick” shaped ureter - as
the distal ureter curves around the enlarged prostate.
Benign prostatic hyperplasia (BPH):
nodules on mri
In the Transitional Zone
(Central Gland)
T2 Heterogenous
Can Restrict Diffusion
May enhance and washout
Post Biopsy Changes
PROSTATE
Classically T1 bright stuff in the gland. It’s subacute blood.
prostate peripheral zone tumor quick
T2 - dark
ADC - dark
Enhancement - early enhancement, eraly washout
prostate peripheral zone hemorrhage quick
T2 - dark (soetomes T1 bright)
ADC - dark (less dark)
Enhancement - none
prostate central/transitional zone tumor quick
T2 - dark ‘charcoal’
ADC - dark
Enhancement - early enhancement, early washout
BPH quick
T2 - dark ‘ well efined’
ADC - less dark
Enhancement - can enhance
Male pelvic cysts lateral
seminal vesicle cyst
diverticulosis of the ampulla of vas deferens
male pelvic midline cysts
prostaticu utricle
mullerian duct cyst
ejaculatory duct cysts
Seminal Vesicle Cyst
overview
The classic look is a unilateral cyst that is lateral to the prostate. If they get large they
can look midline, but if they show you a large one you won’t be able to tell it from a utricle
cyst. They can be congenital or acquired.
Seminal Vesicle Cyst
congenital trivia
- Associated with renal agenesis
- Associated with vas deferens agenesis
- Associated with ectopic ureter insertion
- Associated with polycystic kidney disease
Seminal Vesicle Cyst
acquired trivia
- Obstruction often from prostatic hypertrophy, or chronic infection/scarring
- Classic history is prior prostate surgery
Prostatic Utricle Cyst:
things to know
• This represents a focal dilation in the prostatic urethra (remnant of the Mullerian duct) - as such they communicate with the urethra and can cause “dribbling” (both on and off of
the basketball court).
• Hvpospadias is the most common associated condition which makes sense given the relationship with the urethra.
• Other Associations: Prune Belly Syndrome, Downs, Unilateral Renal Agenesis. and my personal favorite - the Imperforate Anus.
• The tendency towards superinfection is also explained by the communication with the urethra.
• A sneaky trick would be to show it on a RUG, where a prostate utricle cyst would look like a focal out-pouching from the prostatic urethra.
Mullerian Duct Cyst
things to know
- This represents a failed regression of the caudal ends of the Mullerian ducts (male equivalent of the vagina /cervix).
- Does not communicate with the urethra and does not have the same associations as utricle cyst.
This vs That
utricle cyst and mullerian cyst
utricle cyst:
Pear Shaped and Usually Smaller
Will NOT extend above the base o f the prostate
Communicates with the Urethra (JJtricle), therefore could opacify on a RUG
mullerian cyst:
Tear Drop Shaped
Will extend above the base o f the prostate
Does NOT communicate with the Urethra, should not opacify on a RUG
Both have a tiny risk (mostly case reports) o f malignancy (various types: endometrial, clear cell, squamous).
Prostate Abscess
This can cause a thick walled, scptated, heterogenous, cystic lesion
anywhere in the prostate. It is usually bacterial (E. coli). When chronic it can have a more “swiss
cheese” appearance referred to as “cavitary prostatitis.” Usually this is imaged via transrectal
ultrasound - because it gives you (the urologist) the option to do an image guided drain.
Torsion of the Testicle
overview
Results from the testis and spermatic cord twisting within the serosal space leading to ischemia.
If it was 1950 you’d call in your nuclear medicine tech for scintigraphy. Now you just get a Doppler
ultrasound.
Torsion of the Testicle
greyscale
The grey scale findings are fairly straight forward. The testicle is going to be darker (hypo-echoic)
and asymmetrically enlarged - at least in the chronic setting. If it’s chronic then it will shrink up.
Torsion of the Testicle
doppler
The doppler findings are somewhat complex. The most obviously / basic look would be to show you
absent arterial flow. This would be the equivalent of an underhand slow pitch. The curve ball would
be to show you preserved arterial flow BUT with increased resistance and a decreased diastolic flow
(or reversed diastolic flow).
That is correct my friends. Arterial flow does NOT need not be absent for torsion to be
present (depending on the duration and severity). This leads the way for some seriously
fuckery if the test writer wants to be an asshole.
The best way to think about it is like this: Testicle = Brain.
Just like the brain requires continuous diastolic flow (the thing is never off), so does the testicle.
Torsion of the Testicle
three possible patterns
1 - Classic Absence of Arterial Flow
2 - High resistance Arterial Flow (with decreased or reversed diastolic flow)
3 - Monophasic Arterial Waveform (loss of the normal dicrotic notch)
Torsion of the Testicle
stuffery
We are talking about testicular
artery wave forms here. The normal
cremasteric artery will not have diastolic flow
(think about that think as the artery to a
muscle) - it’s normally high resistance.
Torsion of the Testicle
cause
The “bell-clapper deformity,” which describes an abnormal high
attachment of the tunical vaginalis, increases mobility and predisposes to torsion. It is usually a
bilateral finding, so the contralateral side also gets an orchiopexy.
Torsion of the Testicle
viability
The viability is related to the degree of torsion (how many spins), and how long it has
been spun. As a general rule, the surgeons try and get them in the OR before 6 hours.
testicular High Flow States I Hyperemia
If torsion demonstrates decreased flow, it is useful to have an idea about what can
demonstrate increased flow (decreased R.I. or increased diastolic flow)
Two things worth thinking about in this scenario: (1) Epididymo-orchitis (2) Detorsion.
The distinction between these two will be the clinical scenario.
Orchitis is painful. Detorsion is pain free.
Epididymitis
overview
Inflammation o f the epididymis, and the most common cause of acute
onset scrotal pain in adults. In high-school / college age men (likely sexually active men) the
typical cause is chlamydia or gonorrhea. In married men (not likely to be sexually active) it
is more likely to be e-coli, due to a urinary tract source. The epididymal head is the most
affected. Increased size and hyperemia are your ultrasound findings. You can have infection
o f the epididymis alone or infection o f the epididymis and testicle (isolated orchitis is rare).
Epididymitis:
typical spread
Tail ► Body ► Head
Epididymitis:
gamesmanship
Could be asked as “where is the most common location” ? = Tail (because in most cases it starts there).
Orchitis
overview
Typically progresses from epididymitis (isolated basically only occurs from
mumps). It looks like asymmetric hyperemia.
Orchitis
typical
(1) Epididymitis ► (2) Epididymitis + Orchitis
Orchitis
mumps
Straight to Orchitis
Orchitis
impending infarct
The swelling o f the testicle can become so severe that it compromises
venous flow. In this case you will see loss of diastolic flow (or reversal) - similar to the
atypical torsion patterns. This is reported as a sign of “impending infarct.”
Testicular Trauma
overview
The big distinction is rupture vs fracture. Surgical intervention is
required if there is testicular rupture. Intratesticular fracture, and hematomas (small) do not get surgery.
Testicular Trauma
rupture
Disrupted tunica albuginea, heterogenous testicle, poorly defined testicular outline
Testicular Trauma
fracture
Intact tunica albuginea, linear hypoechoic band across the parenchyma o f the testicle, well defined testicular outline.
testicle Epidermoid Cyst
This is a benign mass of
the testicle (no malignant potential), with an Aunt
Minnie “onion skin” look, - alternating
hypoechoic and hyperechoic rings. It’s relatively
non-vascular relative to the rest of the testicle.
Tubular Ectasia of the Rete Testis
This is a common benign finding, resulting from
obliteration (complete or partial) o f the efferent
ducts. It’s usually bilateral - and in older men.
The location of the cystic dilation is next to the
mediastinum testis. Think about this as a normal
variant. It requires no follow up or further
evaluation.
Calcified Vas Deferens
You see this all
the time in bad diabetics.
This can be shown on plain film or CT.
Testicular cancer overview
In general, hypoechoic solid intratesticular masses should be thought of as cancer until
proven otherwise. Doppler flow can be helpful only when it is absent (can suggest
hematoma - in the right clinical setting). If it’s extratesticular and cystic, it’s probably
benign. The step 1 trivia is that cryptorchidism increases the risk of cancer (in both
testicles), and is not reduced by orchiopexy. Most testicular tumors met via the lymphatics
(retroperitoneal nodes at the level o f the renal hilum). The testable exception is
choriocarcinoma, which mets via the blood. Most testicular cancers are germ cell subtypes
(95%) - with seminomas making up about half o f those.
Testicular cancer risk factors
Cryptorchidism (for both testicles), Gonadal Dysgenesis, Klinefelters, Trauma, Orchitis, and testicular microlithiasis (maybe).
Testicular Microlithiasis
This appears as multiple small echogenic
foci within thetestes. Testicular microlithiasis is usually an incidental finding in scrotal US examinations performed for unrelated reasons. It might have a relationship with Germ Cell Tumors (controversial). Follow-up in 6 months, then yearly is probably the recommendation - although this recommendation is controversial.
Testicular Seminoma
This is the most common
testicular tumor, and has the best prognosis as
they are very radiosensitive. They are much more
common (9x) in white people. The classic age is
around 25. It usually looks like a homogenous
hypoechoic round mass, which classically
replaces the entire testicle. On MR1 they are
usually homogeneously T2 dark (nonseminomatous
GCTs are often higher in signal).
Testicular Non-Seminomatous Germ Cell Tumors
Basically this is not a seminoma. We are
talking about mixed germ cell tumors, teratomas, yolk sac tumors, and choriocarcinoma. They
typically occur at a young age relative to seminomas (think teenager). They are more heterogeneous
and have larger calcifications.
Testicular Lymphoma
overview
Just be aware that lymphoma can “hide” in the testes because of the
blood testes barrier. Immunosuppressed patients are at increased risk for developing extranodal/
testicular lymphoma. Almost all testicular lymphomas are non-hodgkin B-cell subtypes. On US, the
normal homogeneous echogenic testicular tissue is replaced focally or diffusely with hypoechoic
vascular lymphomatous tissue.
Testicular Lymphoma
buzzword
multiple hypoechoic masses o f the testicle.
Burned-Out Testicular Tumor
If you see large, dense calcifications with shadowing in the
testicle of an old man this is probably what you should be thinking. The idea is that you’ve had
spontaneous regression of a germ cell testicular neoplasm, that is now calcified. An important pearl
is that there can still be viable tumor in there. Management is somewhat controversial and unlikely
to be asked (most people pull them out).
Testicular cancer
staging pearl
Testicular mets should spread to the para-aortic, aortic, caval region (N1-N3).
It’s an embryology thing.
If you have mets to the pelvic, external iliac, and inguinal nodes - this is considered “nonregional”
i.e. Ml disease. The exception is some kind of inguinal or scrotum surgery was done
before the cancer manifested - but I wouldn’t expect them to get that fancy on the test. Just
remember inguinal / pelvic nodes are non-regional and a higher stage (Ml).
High Yield Tes ticle Tumor Trivia
Seminoma
the most common and has the best prognosis (it melts with radiation)
High Yield Tes ticle Tumor Trivia
Multiple hypoechoic masses
lymphoma
High Yield Tes ticle Tumor Trivia
Homogenous and Microcalcifications
seminoma
High Yield Tes ticle Tumor Trivia
Cystic Elements and Macrocalcifications
Mixed Germ Cell Tumor / Teratoma
High Yield Tes ticle Tumor Trivia
METS
Most testicular tumors met via the lymphatics (choriocarcinoma mets via the blood
- and tends to bleed like stink)
High Yield Tes ticle Tumor Trivia
gynecomastia
can be seen with Sertoli Leydig Tumors
High Yield Tes ticle Tumor Trivia
peutz jeghers
Sertoli Cell Tumors are also seen with Peutz-Jeghers
Testicular cancer
Elevated Beta hCG
Seminoma
Choriocarcinoma (Non-S)
testicular cancer
Elevated AFP
Mixed Germ Cell (Non-S)
Yolk Sac (Non-S)
Male infertility
Obstructive
Congenital bilateral absence o f the vas deferens (seen in Cystic Fibrosis), ejaculatory duct obstruction, prostatic cysts. Think about associated renal anomalies (Zinner Syndrome).
Male infertility
Non-Obstructive
Varicocele, Cryptorchidism, Anabolic Steroid Use, Erectile Dysfunction and “The Liberal Media.”
Varicocele
This is the most common correctable cause of infertility. They can be
unilateral or bilateral. Unilateral is much more common on the left. Isolated right sided
should make you think retroperitoneal process compressing the right gonadal vein.
Cryptorchidism
Undescended testes. The testicle is usually found in the inguinal
canal. The testicle has an increased risk o f cancer (actually they both will - which is weird).
It’s most commonly seen in premature kids (20%).
Major complication association fo r cryptorchidism
- Malignant degeneration - o f both the undescended and contralateral testicle
- Infertility
- Torsion
- Bowel Incarceration - related to the association o f indirect inguinal hernia
Cryptorchidism
gamesmanship
A good distractor would be “orchitis.” It’s a pathology that
involves the balls, so it’s not totally far fetched. Obviously they can get
IV orchitis… but not at a higher rate. It’s not a reported association - so don’t fall
for that.
Zebras and Syndromes Associated With Male Infertility
Pituitary adenoma making prolactin
kallman sydrome (cant smell and infertile)
klinefelter syndrom (tall and gynecomastia and infertile)
zinner syndrome (renal agenesis and ipsilateral seminal vesicle cyst)
Transgender
Gender self identity does not match their genetic / sex assigned identity at
birth. The alternative is a “Cisgender ” - A man who identifies as a man (XY) or a woman who
identifies as a woman (XX). Gender and sexual orientation are different things. Sexual Orientation
is the emotion / sexual attraction to others. Transgender people are not necessarily homosexual.
Gender self identity is different than who you want to fuck.
Transgender Man
A female (XX) who identifies as the masculine (male) gender
Transgender Woman
A male (XY) who identifies as the feminine (female) gender
“Top and Bottom” Surgeries
Slang for breast & genital procedures (gender-affirming surgery)
Vaginoplasty
Procedure to create a functional and cosmetically acceptable neovagina
Penoscrotal inversion (PIV)
The most common procedure with the lowest complication rate. It
involves orchiectomy and “penile disassembly” in a method similar to the induction ceremony of
the feared Unsullied Army. The skin from the disassembled parts is inverted / folded back to
create a tunnel. The clitoris is constructed using the native penile neurovascular anatomy.
Intestinal Interposition
Second line strategy which involves using a segment of bowel (usually
rectosigmoid colon) to create a neovagina by coloperineal anastomosis. They do this because
there uhhh - how best to say this — is “insufficient tissue” from the penis to make the tunnel.
Phalloplasty
overview
Procedure to create a functional and cosmetically acceptable neopenis. Standing
urination is a typical metric of success. Several months prior to constructing the neopenis - these
patients typically undergo hysterectomy (+/- oophorectomy).
Phalloplasty
surgery
Vaginectomy and urethroplasty are performed using vascularized vaginal mucosa to
try and elongate the urethra. Skin flaps often fail - but the “RFFF” or radial flap procedure is
probably the most common. Most of these skin grafts use a “tube in tube” strategy. I can’t believe
the details would be on the exam - but you can imagine they roll the skin and subcutaneous fat up
to make something that looks like a dick. Maybe not the most impressive of dicks - but a dick
none the less. Hey… you know what they say, it’s not the size of the dog in the fight - it’s the
size of the fight in the dog. Not sure if this expression applies to a surgically created neo-phallus
but I’m trying to be positive.
Metoidioplasty
An alternate technique to phalloplasty - which has a lower complication rate.
The downside is the length of the created neopenis is usually not enough to have sex, but they can
still pee standing up (a major metric to success of the procedure). This technique is performed by
first using hormones to hypertrophy the clitoris (like a female body builder). Then the urethra is
lengthened (by dividing various ligaments) and anastomosed to the clitoris, which serves as the
glans. Labia minora is gonna be the source for skin to construct the shaft.
Testicular prostheses / Scrotoplasty
Generally made of silicone (high density on CT) and placed
around 6 month post phalloplasty. Just like the those dick pumps you sometimes see in diabetics -
a hydraulic pump apparatus can be placed - that thing will have tubing and be more water density.
transgender complications
Older technique didn’t resect the vagina - these patients were prone to fistula
between the neourethra and native vagina. DVT / PE is a post op risk if the patient is taking hormone
therapy. Bleeding, infection, urinary complication (urethral stenosis etc) all can occur - as one
might expect.
transgender other usrgeries
that could come up on the exam include breast implants, and the various neck
surgeries to make a dude look less like a dude (thyroid chondroplasty / tracheal shave) and sound
less like a dude (glottoplasty, cricothyroid approximation).
Menstrual Age:
Embryologic Age + 14 days
Embryo
0-10 weeks (menstrual age)
Fetus
> 10 weeks (menstrual age)
Threatened abortion
Bleeding with closed cervix
inevitable abortion
Cervical dilation and/or placental and/or fetal tissue hanging out
incomplete abortion
Residual products in the uterus
complete abortion
All products out
missed abortion
Fetus is dead, but still in the uterus.
Intradecidual Sign
This is the early gestational
sac. When seen covered by echogenic decidua is very
characteristic of early pregnancy. You can see it
around 4.5 weeks. You want to see the thin echogenic
line of the uterine cavity pass by (not stop at) the sac
to avoid calling a little bit o f fluid in the canal a sac.
Double Decidual Sac Sign
This is another positive sign of early pregnancy.
It’s produced by visualizing the layers of decidua.
small amount of fluid between the decidua vera and decidua capsularis
Yolk Sac
This is the first structure visible
within the GS. The classic teaching was you
should always see it when the GS measures
8mm in diameter. The thing should be oval or
round, fluid filled, and smaller than 6 mm.
The yolk sac is located in the chorionic cavity,
and hooked up to the umbilicus o f the embryo
by the vitelline duct.
Yolk Sac gone bad
The yolk sac shouldn’t be too big (> 6 mm), shouldn’t be too small (< 3 mm), and shouldn’t be solid or calcified.
The Amnion
The membranes o f the amniotic sac and chorionic space typically remain separated by a thin layer of fluid, until about 14-16 weeks at which point fusion is normal. If the amnion gets disrupted before 10 weeks the fetus might cross into the chorionic cavity and get tangled up in the fibrous bands. This is the etiology of amniotic band syndrome, which can be terrible (decapitation, limb amputation, etc...).
Double Bleb Sign
This is the earliest visualization o f the embryo. This is two fluid filled sacs (yolk and amniotic) with the flat embryo in the middle.
yolk sac
early embryo
anmiotic sac
placenta site
Crown Rump Length
This is typically used to estimate gestational age, and is more
accurate than menstrual history. * Embryo is normally visible at 6 weeks.
Anembryonic Pregnancy
A gestational sac without an embryo. When you see this,
the choices are (a) very early pregnancy, or (b) non-viable pregnancy. The classic teaching
was you should see the yolk sac at 8 mm (on TV). Just remember that a large sac (>8-10
mm) without a yolk sac, and a distorted contour is pretty reliable for a non-viable pregnancy
Pseudogestational Sac
This is not the same thing as an anembryonic pregnancy. This is seen in the presence of an ectopic pregnancy. What you are seeing is a little bit of blood in the uterine cavity with surrounding bright decidual endometrium (charged up from the pregnancy hormones).
Subchorionic Hemorrhage
These are very common. The thing to know is that the
percentage o f placental detachment is the prognostic factor most strongly associated with
fetal demise; hematoma greater than 2/3 the circumference o f the chorion has a 2x increased
risk of abortion. Other trivia: women older than 35 have worse outcomes with these.
Implantation Bleeding
This is a nonspecific term referring to a small subchorionic
hemorrhage that occurs at the attachment o f the chorion to the endometrium.
Diagnostic of Pregnancy Failure
Crown-rump length of >7 mm and no heartbeat
Mean sac diameter of >25 mm and no embryo
No embryo with heartbeat >2 wk after a scan that showed a gestational sac without a yolk sac
No embryo with heartbeat >11 days after a scan that showed a gestational sac with a yolk sac
Suspicious for Pregnancy Failure
No embryo > 6 wk after last menstrual period
Mean sac diameter of 16-24 mm and no
embryo
No embryo with heartbeat 13 days after a scan that showed a gestational sac without a yolk sac
No embryo with heartbeat 10 days after a scan that showed a gestational sac with a yolk sac
Pregnancy of Unknown Location
overview
This is the vocabulary used when neither a normal IUP or ectopic pregnancy is identified in the setting of a positive b-hCG. Typically this just means it is a very very early pregnancy, but you can’t say that with certainty.
Pregnancy of Unknown Location
possibilities
1 - Normal Early Pregnancy
2 - Occult Ectopic
3 - Complete Miscarriage
Pregnancy of Unknown Location
The management is follow up (serial b-hCG) and repeat US — assuming the patient is hemodynamically stable.
High Risk for Ectopic
Hx o f PID, Tubal Surgery, Endometriosis, Ovulation Induction, Previous Ectopic, Use o f an IUD.
Ectopic pregnancy locations
The majority of ectopic pregnancies (nearly 95%) occur in the fallopian tube (usually the
ampulla). A small percentage (around 2%) are “interstitial” developing in the portion o f the
tube which passes through the uterine wall. These interstitials are high risk, as they can grow
large before rupture and cause a catastrophic hemorrhage. It is also possible (although very
rare) to have implantation sites in the abdominal cavity, ovary, and cervix.
Ectopic Bhcg
Always start down the ectopic pathway with a positive BhCG. At around 1500-2000 mlU/L you should see a gestational sac. At around 5000 mlU/L you should see a yolk sac. As a general rule, a normal doubling time makes ectopic less likely.
Tubal Ring Sign
An echogenic ring, which surrounds an un-ruptured ectopic pregnancy. This is an excellent sign of
ectopic pregnancy - and has been
described as 95% specific.
Heterotopic Pregnancy
This is a
baby in the uterus and a baby in the tube (or other ectopic location). This is pretty
rare, and typically only seen in women
taking ovulation drugs, or with prior bad
PID.
The Big 3 to Remember with Ectopics (positive B-hCG)
(1) Live Pregnancy / Yolk Sac outside the uterus = Slam Dunk
(2) Nothing in the uterus + anything on the adnexa (other than corpus luteum) =
75-85% PPV for ectopic
a. A moderate volume o f free fluid increases this to 97% PPV
(3) Nothing in the uterus + moderate free fluid = 70% PPV
a. More risk if the fluid is echogenic
Fetal Biometry and Fetal Growth
In the second and third trimesters, four standard measurements of fetal growth are made (Biparietal, Head Circumference, Abdominal Circumference, and Femur Length). The testable trivia seems to include what level you make the measurement, and what is and is not included (see chart).
Fetal Measurement For Growth
Biparietal Diameter
“BPD”
Recorded at the level of the thalamus from the outermost edge of the near skull to the inner table of the far skull
Affected by the shape of the fetal skull (false large from bachycephaly, false small form dolichocephaly
Fetal Measurement For Growth
Head Circumference
Recorded at the same slice as BPD
Does NOT include the skin
Affected less by head shape
Fetal Measurement For Growth
Abdominal Circumference
Recorded at the level o f the junction o f the umbilical vein and left portal vein
Does NOT include the subcutaneous soft
tissues
Fetal Measurement For Growth
Femur Length
Longest dimension of the femoral shaft
Femoral epiphysis is NOT included
Estimated Fetal Weight
This is calculated by the machine based or either (1) BPD and AC, or (2) AC and FL.
Gestational Age (GA)
Ultrasound estimates o f gestation age are the most accurate in early pregnancy (and become less precise in the later portions). Age in the first trimester is made from crown rump length. Second and third trimester estimates for age are typically done using BPD, HC, AC, and FL - and referred to as a “composite GA.”
Gestation Age (Less Good Later in the Pregnancy)
First Trimester - Crown Rump Length
Accurate to 0.5 weeks
Gestation Age (Less Good Later in the Pregnancy)
2nd and 3rd Trimester - “Composite GA”
Accurate to 1.2 weeks (between 12 and 18 weeks)
Accurate to 3.1 weeks (between 36 and 42 weeks)
Readings Suggestive of IUGR
- Estimated Fetal Weights Below 10th percentile
- Femur Length / Abdominal Circumference Ratio (F /AC) > 23.5
- Umbilical Artery Systolic / Diastolic Ratio > 4.0
Readings Suggestive of IUGR
Not A ll is lost
If the kid is measuring small, he might just be a little guy. If he has normal Doppler studies - most of the time they are ok.
Readings Suggestive of IUGR
Maybe All is lost
If the kid is measuring small, suggesting IUGR, and he has oligohydramnios (AFI < 5) or polyhydramnios, he/she is probably toast.
Readings Suggestive of IUGR
Trivia
Most common cause for developing oligohydramnios during the 3rd trimester =
Fetal Growth Restriction associated with Placental Insufficiency.
Intrauterine Growth Restriction
Asymmetric overview
Think about this as a restriction o f weight followed by length. It is the more common o f the two types. The head will be normal in size, with the body being small. Some people call this “head sparing,” as the body tries to protect the
brain. You see this mainly in the third trimester, as a result o f extrinsic factors.
Intrauterine Growth Restriction
Asymmetric classic scenario
The classic scenario would be normal growth for the first two trimesters, with a normal head / small body (small abdominal circumference) in the third trimester - with a mom having chronic high BP / pre-eclampsia.
Intrauterine Growth Restriction
Asymmetric causes
There are a bunch o f causes. I recommend remembering these three: High BP, Severe Malnutrition, Ehler-Danlos.
Intrauterine Growth Restriction
Symmetric overview
This is a global growth restriction, that does NOT spare the head. This is seen throughout the pregnancy (including the first trimester). The head and body are both small. This has a much worse prognosis, as the brain doesn’t develop normally.
Intrauterine Growth Restriction
Symmetric causes
There are also a bunch o f causes. I recommend remembering these: TORCH infection, Fetal Alcohol Syndrome / Drug Abuse, Chromosomal Abnormalities, and Anemia.
Symmetric IUGR
acronym
- Small Head
- Skinny Body
- Same Throughout Pregnancy
- Syphilis (Among other TORCHs)
- Scotch Whiskey (Fetal EtOH)
- Some Extra Chromosomes
Asymmetric IUGR
acronym
- Abdomen is small
- Aching Belly (Malnutrition)
- Abnormally High BP
- “Alastic” skin (Ehler Danlos)
- Asymmetric Time Interval (primarily seen in 3rd trimester)
Umbilical Artery Systolic I Diastolic Ratio
overview
The resistance in the umbilical artery should progressively decrease with gestational age. The general rule is 2-3 at 32 weeks. The ratio should not be more than 3 at 34 weeks. An elevated S/D ratio means there is high resistance. High resistance patterns are seen in pre-eclampsia and IUGR. Worse than an elevated ratio, is absent or reversed diastolic flow - this is associated with a very poor prognosis.
Umbilical Artery Systolic I Diastolic Ratio
the way i remember this
I think about the kid starting out as a clump of cells/mashed up soup.
Early on he/she is basically just a “muscle.” Then as he/she gets closer and closer to viable age he/she becomes more like a “brain.” Once you think about it like that - muscle vs brain, it’s much easier to understand why the diastolic flow goes up (S/D ratio goes down).
Umbilical Artery Systolic I Diastolic Ratio
remember
Remember the brain is always on, so it needs continuous flow. Muscles are only on when you need to perform amazing feats of strength. So more brain = more diastolic flow. This also explains why absent or reversed diastolic flow is so devastatingly bad. In fact, the evil socialist health care systems in Europe use carotid ultrasound as a cheap brain death test (no diastolic flow in the ICA = brain dead). Coincidently, the absence of diastolic flow in the ICA is also used in many American Radiology Departments as hiring criteria for the QA Officer.
Biophysical Profile:
This thing was developed to look for acute and chronic hypoxia. Points are assigned (2 for normal, 0 for abnormal). A score of 8-10 is considered normal. To call something abnormal, technically you have to be watching for 30 mins.
Components of Biophysical Profile
Amniotic Fluid: At least 1 pocket measuring > 2 cm in a vertical plane: Assess Chronic Hypoxia
Fetal Movement: 3 discrete movements: Assess Acute Hypoxia
Fetal Tone: 1 episode of fetal extension from flexion: Assess Acute Hypoxia
Fetal Breathing: 1 episode of “Breathing motion” lasting 30 sec: Assess Acute Hypoxia
Non-stress Test: 2 or more fetal heart rate accelerations of at least 15 beats per minute for 30 seconds or longer: Assess Acute Hypoxia
Macrosomia
Babies that are too big (above the 90th percentile). Maternal diabetes (usually gestational, but could be type 2 as well), is the most common cause. As a point of trivia, type 1 diabetic mothers can also have babies that are small secondary to hypoxia from microvascular disease of the placenta. The big issue with being too big is complications during delivery (shoulder dystocia, brachial plexus injury) and after delivery (neonatal hypoglycemia, meconium
Erb’s Palsy
Injury to the upper trunk of the brachial plexus (C5-C6), most commonly seen in shoulder dystocia (which kids with macrosomia are at higher risk for aspiration).
If you see an aplastic or hypoplastic humeral head / glenoid in a kid, you should immediately think about an Erbs Palsy.
Clinical Correlation Recommended.
Amniotic Fluid overview
Early on, the fluid in the amnion and chorionic spaces is the result of filtrate from the membranes. After 16 weeks, the fluid is made by the fetus (urine). The balance of too much (polyhydramnios) and too little (oligohydramnios) is maintained by swallowing of the urine
and renal function. In other words, if you have too little fluid you should think kidneys aren’t working. If you have too much fluid you should think swallow or other GI problems. Having said that, a common cause of too much fluid is high maternal sugars (gestational diabetes). Fine particulate in the fluid is normal, especially in the third trimester.
Amniotic Fluid Index
measuremnents
Made by measuring the vertical height of the deepest fluid
pocket in each quadrant of the uterus, then summing the 4 measurements.
Amniotic Fluid Index
normal
Normal is 5-20.
Amniotic Fluid Index
oligohydramnios
-AFI < 5
Not Pee’n Enough-Bad Kidneys
Amniotic Fluid Index
polyhydramnios
-AFI > 20 or
-Single Pocket > 8 cm
Not Drinking Enough Pee-Bad Gl
Normal Development
Brain
Choroid plexus is large and echogenic. There should be less than 3 mm of separation o f the choroid plexus from the medial wall o f the lateral ventricle (if more it’s ventriculomegaly). The cistema magna should be between 2 mm-11 mm (too small think Chiari II, too large think Dandy Walker).
Normal Development
Face/neck
The “fulcrum” of the upper lip is normal, and should not be called a cleft lip.
Normal Development
lungs
The lungs are normally homogeneously echogenic, and similar in appearance to the liver.
Normal Development
heart
The only thing to know is that papillary muscle can calcify “Echogenic Foci in the ventricle,” and although this is common and can mean nothing - it’s also associated with an increased risk o f Downs (look hard for other things).
Normal Development
abdominal
If you only see one artery adjacent to the bladder, you have yourself a two vessel cord. Bowel should be less than 6mm in diameter. Bowel can be moderately echogenic in the 2nd and 3rd trimester but should never be more than bone. The adrenals are huge in newborns, and are said to be 20 x their relative adult size.
Two Vessel Cord - Gamesmanship
There are two main ways to show a two vessel cord. The first one is a single vessel running lateral to the bladder down by the cord insertion. The second is to show the cord in cross section with two vessels.
Cystic Rhombencephalon
The normal rhombencephalon is present
as a cystic structure in the posterior fossa
around 6 - 8 weeks.
D o n ’t call it a Dandy-Walker
malformation, for sure that will be a
distractor.
Physiologic Midgut Herniation
The midgut normally herniates into the umbilical cord around 9-11 weeks.
Don ’/ call it an omphalocele, for sure that will be a distractor.
Placenta and cord
normal
You can first start to see the placenta around 8 weeks (focal thickening along the periphery o f the gestational sac). It should be shaped like a disc around 12 weeks. The normal sonographic appearance is “granular” with a smooth cover (the chorion). Underneath
the basal surface there is a normal retroplacental complex o f decidual and myometrial veins.
Placenta and cord
normal
You can first start to see the placenta around 8 weeks (focal thickening along the periphery o f the gestational sac). It should be shaped like a disc around 12 weeks. The normal sonographic appearance is “granular” with a smooth cover (the chorion). Underneath the basal surface there is a normal retroplacental complex o f decidual and myometrial veins.
Placenta and cord
Normal Placental Aging
As the placenta ages it gets hypoechoic areas, septations, and randomly distributed calcifications.
Placenta and cord
Venous Lakes
These are an incidental finding o f no significance. They look like focal hypoechoic areas under the chorionic membrane (or within the placenta). You can sometimes see slow flow in them.
Variant Placental Morphology
Bilobed placenta
Succenturiate lobe
Circumvallate placenta
Bilobed placenta
Two near equal sized lobes - connected by a thin strip.
Increased risk o f type 2 vasa previa (vessel cross the internal os), post partum hemorrhage from retained placental tissue, and velamentous insertion of the cord
Succenturiate Lobe
One or more small accessory lobes
Increased risk o f type 2 vasa previa, post partum hemorrhage from retained placental tissue
Circumvallate Placenta
Rolled placental edges with smaller chorionic plate
High risk for placental abruption and IUGR
Placental Thickness
too thin
<1 cm
Placental Insufficiency, Maternal Hypertension, Maternal DM, Trisomy 13, Trisomy 18, Toxemia o f Pregnancy
Placental Thickness
too thick
> 4cm
Fetal Hydrops, Maternal DM, Severe Maternal Anemia, Congenital Fetal Cancer, Congenital Infection. Placental Abruption
Placental Abruption
Painful
Placental Abruption
buzzword
Myometrial Contractions / Fibroids will displace the retroplacental complex
THIS vs THAT: Placental Abruption vs Myometrial Contraction I Fibroid
Placental Abruption will disrupt the retroplacental complex o f blood vessels
Placenta Previa:
overview
Painless
This is a low implantation of the placenta that covers part of or all of the internal cervical os. A
practical pearl is that you need to have an empty bladder when you look for this (full bladder
creates a false positive). Several subtypes - as seen in my awesome little chart below.
Placenta Previa:
buzzword
“painless vaginal bleeding in the third trimester.”
Placenta Previa:
low lying
Margin is within 2 cm of the internal cervical os
Placenta Previa:
marginal
Extends to the edge of the internal cervical os (but doesn’t cover it)
Placenta Previa:
complete
covers the internal os
Placenta Previa:
central
centered of the internal os
Placenta Creta
This is an abnormal insertion of the placenta, which invades the myometrium. The severity is graded with fancy sounding Latin names. The risk factors include prior C-section, placenta previa, and advanced maternal age. The sonographic appearance varies depending on the severity, but generally speaking you are looking for a “moth-eaten” or “Swiss cheese” appearance o f the placenta, with vascular channels extending from the placenta into the myometrium (with turbulent flow on Doppler). Thinning of the myometrium (less than 1mm) is another sign. This can be serious business, with life
threatening bleeding sometimes requiring hysterectomy.
Placenta Creta
Risk factors
Risk factors are prior c-section. and placenta previa
Placenta Accreta
Most common (75%) and mildest form. The villi attach to the myometrium, without invading.
Placenta Increta
Villi partially invade the myometrium
Placenta Percreta
The really bad one. Villi penetrate through the myometrium or beyond the serosa. Sometimes there is invasion of the bladder or bowel.
Placenta creta
lating
“Ad” = To (accreta)
“In “ = Into (increta)
“Per” = Through (percreta)
Placenta Chorioangioma
This is basically a hamartoma of the placenta, and is the most common benign tumor of the placenta. These are usually wellcircumscribed hypoechoic masses near the cord insertion. Flow
within the mass pulsating at the fetal heart rate is diagnostic (they arc perfused by the fetal circulation). They almost always mean nothing, but if they are large (> 4 cm) and multiple (“choriangiomatosis”) they can sequester platelets, and cause a high output failure (hydrops).
THIS vs THAT: Placental Chorioangioma vs Placental Hematoma
Chrorioangioma has pulsating Doppler flow
Hematoma does NOT
Normal Cord
Should have 3 vessels (2 arteries, 1 vein).
Two Vessel Cord
This is a normal variant - seen in about 1% of pregnancies. Usually the
left artery is the one missing. This tends to occur more in twin pregnancies and maternal diabetes. There is an increased association with chromosomal anomalies and various fetal malformations (so look closely). Having said that, in isolation it doesn’t mean much.
Velamentous Cord Insertion
This is the term for when the cord inserts into the fetal membranes outside the placental margin, and then has to travel back through the membranes to the placenta (between the amnion and the chorion). It’s more common with twins, and increases the risk of intra-uterinc growth restriction and growth discordance among twins.
Marginal Cord Insertion
This is basically almost a velamentous insertion (cord is within 2 cm of the placental margin). It’s also seen more in twin pregnancies.
Vasa Previa
Fetal vessels that cross (or almost cross) the internal cervical os. It’s seen more
in twin pregnancies, and variant placental morphologies. There arc two types:
- Type 1: Fetal vessels connect to a velamentous cord insertion within the main placental body
- Type 2: Fetal vessels connect to a bilobcd placenta or succenturiate lobe.
Nuchal Cord
This is the term used to describe a cord wrapped around the neck of the fetus. Obviously this can cause problems during delivery
Umbilical Cord Cyst
These arc common (seen about 3% of the time) and are usually single (but can be multiple). As a point of completely irrelevant trivia, you can divide these into
false and true cysts. True cysts are less common, but have fancy names so they are more likely to be tested. Just know that the omphalomesenteric duct cyst is usually peripheral, and the allantoic
cyst is usually central. If the cysts persist into the 2nd or 3rd trimester then they might be associated with trisomy 18 and 13. You should look close for other problems.
Down syndrome
Congenital Heart Disease
More than half o f fetuses (or feti, if you prefer) with Downs have congenital heart issues, - most commonly AV canal and VSD
Down syndrome
Duodenal Atresia
Most common intra abdominal pathology associated with Downs (hard to see before 22 weeks)
Down syndrome
Short Femur Length
Not specific
Down syndrome
Echogenic Bowel
Not Specific (can be seen with obstruction, infection, CF, ischemia, and lots o f other stuff)
Down syndrome
Choroid Plexus Cyst
Not Specific, and actually seen more with Trisomy 18. It should prompt a close survey for other findings (normal if in isolation)
Down syndrome
Nuchal Translucency
Translucency > 3mm in the first trimester,
Down syndrome
Nuchal Fold Thickness
Thickness > 6mm in the second trimester- nonspecific and can also be seen with Turners
Down syndrome
Echogenic Focus in Cardiac Ventricle
Not Specific, but increased risk o f Downs x 4
Nuchal Lucency:
Measured between 9-12 weeks, this anechoic area between the neck/ occiput and the skin should be less than 3 mm.
Measurements > 3 mm are associated with Downs (trisomy 2 1 ) or other chromosomal abnormalities. Positioning of the neck is critical to avoid false
positives. The ideal positioning is a neutral neck, with the nasal bone visualized, and the head in the mid-sagittal position. A well delineated skin edge. Maternal blood sample also analyzed for free Beta hCG and pregnancy associated plasma protein-A (PAPP-A).
Amniotic Band Syndrome
overview
The fetus needs to stay in the amniotic cavity, and stay the hell out of
the chorionic cavity. If the amnion gets disrupted and the fetus wanders
/ floats into the chorionic cavity he/she can get caught in the sticky
fibrous septa. All kinds of terrible can result ranging from decapitation,
to ann/leg amputation.
Amniotic Band Syndrome
This is most likely to be shown in one of two ways
(1) X-ray of a hand or baby gram showing fingers amputated or a hand/arm amputated - with the remaining exam normal, or
(2) Fetal ultrasound with the bands entangling the arms or legs of a fetus.
Hydrops
overview
Fetal hydrops is bad news. This can be from immune or non-immune causes. The most common
cause is probably Rh sensitization from prior pregnancy. Some other causes include; TORCHS,
Turners, Twin Related Stuff, and Alpha Thalassemia. Ultrasound diagnosis is made by the
presence of two of the following: pleural effusion, ascites, pericardial effusion, and
Subcutaneous Edema. A sneaky trick is to instead show you a thickened placenta (> 4-5cm)
“placentomegaly” - they call it, although I think it’s much more likely to show a pleural effusion
and pericardial effusion.
Hydrops
quick
Body Wall Edema, Pleural Effusion, Ascites
-C h ia r i II / Open N e u ra l T u b e D e fe c t
I think at least some general idea of the mechanism for this pathology is helpful for
understanding the ultrasound findings. There are a bunch of purposed mechanisms, and of
course they all think they are right. I don’t give a shit which one is the “real mechanism,” I
just picked the one that helps me understand the findings.
So this is the one I like: You have a hole in your back from a neural tube defect (Step 1 trivia
= not enough folate). The hole in your back (“myelomeningocele”) lets CSF drip out. So
you end up with a low volume o f CSF. The CSF volume needs to be at a certain pressure to
distend the ventricular system. If it’s under distended then the hindbrain structures drop into
a caudal position. This caudal herniation of the cerebellar vermis, brainstem, and 4th
ventricle is the hallmark o f Chiari II.
This caudal herniation o f the cerebellum into the foramen magnum obliterate the normal
contour of the vermis, creating the contour o f a banana.
If you can think about a normal pressure in the developing ventricular system being
necessary for the brain to stretch into a normal shape, then it isn’t a far stretch to think about
this normal pressure being needed to shape the skull correctly, too. The low pressure and
abnormal distention of the developing brain results in incomplete stretching of the postal
(front part) skull. The result is a “lemon shaped” rostral skull. The key point (testable) is
that this lemon shape goes away in the 3rd trimester. So it’s only present in the 2nd trimester.
The way I remember this is that the problem was from a lack o f volume. Once the brain
grows big enough (even if there isn’t enough CSF distention) it still gets big enough to put a
normal curve on that rostral skull. So they “grow” out o f it.
-C h ia r i II / Open N e u ra l T u b e D e fe c t
testable trivia
- Both banana and lemon signs are classic for the Chiari II / Spina Bifida Path
- The banana sign is present in both 2nd and 3rd trimesters
- The lemon sign is only in the 2nd trimester (you grow out o f it).
- The banana sign is more sensitive and specific
- The lemon sign is less sensitive and specific; it can also be seen in Dandy Walker, Absent Corpus Callosum, Encephaloceles, etc… Having said that if you see it on the test it’s Chiari 2 + Open NTD.
- Hydrocephalus is also seen with Chiari II + Open NTD - but only later in gestation, and only when it’s severe.
Banana
-Loss of the normal bilobed shaped of the cerebellum
Lemon
-Flat / Concave Frontal Bones
Ventriculomegaly
overview
There are multiple causes including hydrocephalus (both communicating and non-communicating), and cerebral atrophy. Obviously this is bad, and
frequently associated with anomalies.
Ventriculomegaly
things to know
- Aqueductal Stenosis is the most common cause o f non-communicating hydrocephalus in a neonate
- Ventricular atrium diameter > 10 mm = too big
- “Dangling choroid” hanging off the wall more than 3 mm = too big
V e n tric u lom e g a ly - S h o w s
dangling choroid
Choroid Plexus Cyst
This is one o f those incidental findings
that in isolation means nothing. Having
said that, the incidence o f this finding is
increased in trisomy 18. trisomy 2 1 ,
Turner’s Syndrome, and Klinefelter
Syndrome.
Facial Clefts
This is the most common fetal facial anomaly. About 30% of the time
you are dealing with chromosome anomalies. Around 80% of babies with cleft lips have
cerebral palsy. You can see cleft lips, but cleft palate (in isolation) is very hard to see.
Cystic Hygroma
If they show you a complex cystic mass in the posterior neck, in the antenatal period, this is the answer. The follow-up is the association with Turners and Downs.
Anencephaly
This is the most common neural tube defect. You have total absence of
the cranial vault and brain above the level of the orbits. Obviously this is not compatible with life.
Anencephaly quick
no brain/vault above the orbits
Congenital Diaphragmatic Hernia
Abdominal contents push into the chest.
Nearly all are on the left (85%). The things to know is that it (1) causes a high mortality because o f its association with pulmonary hypoplasia, and (2 ) that all the kids are malrotated (it messes with normal gut rotation). If they show this it will either be (a) a newborn chest x-ray, or (b) a 3rd trimester MRI.
Echogenic Intracardiac Focus (EIF)
This is a calcification seen in a papillary
muscle (usually in the left ventricle). You see them all the time, they don’t mean that much but are seen at a higher rate Trisomy 21 (12%) and Trisomy 13. So you are supposed to look for more features.
Echogenic Intracardiac Focus (EIF)
highest yield trivia
- It occurs in the normal general population - around 5%,
* It occurs more in Downs patients around 12%.
Abnormal Heart Rate
Tachycardia is defined as a rate > 180 bpm. Bradycardia is defined as a rate < 100 bpm.
Double Bubble
This is described in detail in the Peds Chapter.
Just realize this can be shown with antenatal
ultrasound or MRI. It’s still duodenal atresia.
Echogenic Bowel
This can be a normal variant but can also be associated with significant badness. Normally bowel is isoechoic to the liver. If it’s equal to the iliac crest bone then it’s too bright. The DDx includes CF, Downs and other Trisomies, Viral Infections, and Bowel Atresia.
Sacrococcygeal Teratoma
This is the most common tumor of the fetus or infant. These solid or cystic masses are typically large and found either on prenatal imaging or birth. They can cause mass effect on the GI system, hip dislocation, nerve compression causing incontinence, and high output cardiac failure. Additionally, they may cause issues with premature delivery, dystocia, and hemorrhage o f the tumor. They are usually benign (80%).
Those presenting in older infants tend to have a higher malignant potential. The location of the mass is either external to the pelvis (47%), internal to the pelvis (9%), or dumbell’d both inside and outside (34%).
Autosomal Recessive Polycystic Kidney Disease
The classic look is massively enlarged bilateral kidneys with oligohydramnios. Additional details in the Peds chapter.
Posterior Urethral Valves
The classic look is bilateral hydro on either fetal US or 3rd Trimester MRI.
Short Femur
A short femur (below the 5th percentile) can make you think o f a skeletal dysplasia.
Incompetent Cervix
When shortened, the cervix is associated with a high risk of premature delivery. You call it short when the endocervical canal is < 2.5 cm in length.
Hydronephrosis
occurs in 80% of pregnancies (mechanical compression of the ureters is likely the cause). It tends to affect the
right more than the left (dextrorotation of the pregnant uterus).
Things That Grow During Pregnancy:
- Babies
- Splenic Artery Aneurysms
- Renal AMLs
- Fibroids
Uterine Rupture
You see this most commonly in the 3rd trimester at the site of prior csection.
Other risk factors worth knowing are the unicomuate uterus, prior uterine curettage, “trapped uterus’’ (persistent retroflexion from adhesions), and interstitial implantation.
HELLP Syndrome
Hemolysis, Elevated Liver Enzymes, Low Platelets. This is the most severe form of pre-eclampsia, and favors young primigravid women in their 3rd trimester. It’s bad news and 20-40% end up with DIC. If they are going to show this, it will be as a subcapsular hepatic hematoma in pregnant (or recently pregnant) women.
Peripartum Cardiomyopathy
This is a dilated cardiomyopathy that is seen in the last month of pregnancy to 5 months postpartum. The cardiac MRI findings include a global depressed function, and non-vascular territory subepicardial late Gd enhancement - corresponding to cellular lymphocytic infiltration.
Sheehan Syndrome
This is pituitary apoplexy seen in postpartum female who suffer from large volume hemorrhage (causing acute hypotension). The pituitary grows during pregnancy, and if you have an acute hypotensive episode you can stroke it out (it bleeds). The look on MR is variable depending on the time period, acute it will probably be T1 bright (if they show a picture). Ring enhancement around an empty sella is a late look.
Ovarian Vein Thrombophlebitis
This can be a cause of postpartum fever. Risk factors include C-section and endometritis. The right side is affected five times more often than the left. They could show you an enlarged ovary and a thrombosed adjacent ovarian vein.
Retained Products of Conception
The typical clinical story is continued bleeding after delivery (or induced abortion). The most common appearance is an echogenic mass within the uterine cavity. The presence or absence of flow is variable, you can have lots or you can have none. A sneaky way to show this is irregular thickening of the endometrium (> 1 0mm) with some reflective structures and shadowing - representing the fetal parts. You can also think about RPOC when the endometrial thickness is > 5 mm following dilation and curettage. Testable associations include: medical termination of pregnancy (abortion), second trimester miscarriage, and placenta accreta.
Endometritis
Broadly speaking, it is an inflammation or infection o f the endometrium. The history will be (if you are given one) fever, and uterine tenderness and recent c-section (or prolonged labor). On ultrasound you will see a thickened, heterogenous endometrium, with or without fluid / air.
Placentation Terminology
So you can have monozygotic twins (identical) or dizygotic
twins (not-identical). The dizygotics are always dichorionic and diamniotic. The placenta of the
monozygotics is more variable and depends on the timing of fertilized ovum splitting (before 8 days =
diamniotic, after 8 days = monoamniotic). As a point of trivia, a late splitting (after 13 days) can
cause a conjoined twin. As a general rule, the later the split the worse things do (monoamniotics have
more bad outcomes - they get all tangled up, and the conjoined ones have even more problems).
Membrane Thickness
To differentiate the different types, some people use a method classifying
thin and thick membranes. Thick = “easy to see” 1-2 mm, Thin = “hard to see.” Thick is supposed
to be 4 layers (dichorionic). Thin is supposed to be 2 layers (monochorionic). Obviously this
method is very subjective.
Twin-Peak Sign
A beak-like tongue between the two membranes of dichorionic diamniotic
fetuses. This excludes a monochorionic pregnancy.
T Sign
Think about this as basically the absence of the twin peak sign. You don’t see chorion
between membrane layers. T sign = monochorionic pregnancy.
Twin peack sing =
dichorionic
t sign =
monochorionic
Twin Growth
You can use normal growth charts in the first and second trimester (but
not the third). The femur length tends to work best for twin age in later pregnancy. More
than 15% difference in fetal weight or abdominal circumference between twins is considered
significant.
Twin- Twin Transfusion
This occurs in monochorionic twins when a vascular
communication exists in the placenta. You end up with one greedy fat twin who takes all the
blood and nutrients, and one skinny wimpy looking kid who gets the scraps. The somewhat
counter intuitive part is that the skinny kid actually does better, and the fat one usually gets
hydrops and dies. You are going to have unequal fluid in the amniotic sacs, with the donor
(skinny) twin having severe oligohydramnios and is sometimes (*buzzword) “stuck to the
wall of the uterus,” or “shrink w rapped.” The fat twin floats freely in his polyhydramniotic
sac. The donor (skinny) twin will also have a high resistance umbilical artery.
Twin Reversed Arterial Perfusion Syndrome
You can get intraplacental
shunting that results in a “pump twin” who will pump blood to the other twin. The other
twin will not develop a heart and is typically referred to as an “acardiac twin.” The acardiac
twin will be wrecked (totally deformed upper body). The “pump twin” is usually normal,
and does ok as long as the strain on his/her heart isn’t too much. If the acardiac twin is really
big (> 70% estimated fetal weight o f the co-twin) then the strain will usually kill the pump
twin. They could show this as a Doppler ultrasound demonstrating umbilical artery flow
toward the acardiac twin, or umbilical vein flow away from the acardiac twin (opposite of
normal flow).
One Dead Twin
At any point during the pregnancy one of the twins can die. It's a bigger problem (for the surviving twin) if it occurs later in the pregnancy. “Fetus Papyraceous” is a fancy sounding Latin word for a pressed flat dead fetus.
“Twin-Embolization Syndrome”
when you have embolized, necrotic, dead baby
being transferred to the living fetus (soylent green is people!). This can result in D1C, tissue
ischemia, and infarct. By the way, a testable point is that this transfer can only occur in a
monochorionic pregnancy.
