This document discusses imaging in male infertility. It describes how scrotal ultrasound can evaluate the testes and surrounding structures for conditions like varicocele, testicular atrophy, and torsion. Transrectal ultrasound and MRI can further assess the prostate and ductal system. Common causes of male infertility include varicocele, infections leading to obstruction, testicular issues like microlithiasis or cancer, and hormonal conditions. Imaging helps identify structural abnormalities and guide diagnosis and management of infertility.

1. 17/10/2023
IMAGING IN INFERTILITY
PRESENTER : DR. KEERTHI REDDY A
MD RADIODIAGNOSIS PG 2nd YR
OSMANIA MEDICAL COLLEGE & HOSPITALS
MODERATOR : DR. SUSHMA CHARY MAM
1

2. • Infertility is defined as failure to achieve a pregnancy after 12
months or more of regular unprotected sexual intercourse.
• Primary infertility- who never conceived.
• Secondary infertility- who had previous pregnancy but failure
to conceive subsequently.
• Sterility usually refers to inability to produce a live child
sterility sterility usually refers to inability to sterility usually refers to inability to
produce a live child a live sterility usually refers to inability to produce a live
child refers to inability to sterility usually refers to inability to produce a sterility
usually refers to inability to produce a live child sterility usually refers to inabilit
to produce a live child a live child
2
2

3. Imaging in MALE INFERTILITY
• Scrotal ultrasound is useful in the evaluation of the
testicles and extratesticular scrotal structures (i.e.,
epididymis, peritesticular veins, and spermatic
cord,scrotal wall)
• Transrectal ultrasound (TRUS) and MRI can yield
pertinent information about the distal ductal
system and prostate gland. MRI is also used to
evaluate the brain and sella turcica in cases in
which an abnormality of these areas is suspected
on the basis of hormonal assays.
3

4. 4
• We should carefully examine the man’s body habitus and
perform a complete genitourinary examination .
• Next, a semen analysis report is to be checked if it’s
already done.
Volume >1.5ml Conc.> 15million/ml
total progressive
and nonprogressive
motility >40%
Normal
morphology >4%
Aspermia
Azoospermia Asthenozoospermia Teratozoospermia
Hypospermia Oligozoospermia Necrotozoospermia
Hyperspermia Polyzoospermia
Leucospermia
Hematospermia
4

5. 5
Nonobstructive
disease(a
ff
ecting sperm
production/function)
• cryptorchidism
• primary testicular failure
• varicocele
• endocrinopathy
• chromosomal abnormality
• anabolic steroid abuse
• gonadotoxin exposure
The various causes of male infertility can be
subcategorized as obstructive and
nonobstructive azoo- or hypospermia.
Obstructive
disorders(preventing the
delivery of sperm)
• congenital bilateral absence
of the vas deferens
• ejaculatory duct obstruction
• prostatic cysts
5

6. 6
6

7. • Non obstructive causes
Pretesticular Testicular
Primary Hypogonadism
(Hypergonadotropic
Hypogonadism)
Varicocoele
Testicular atrophy
Orchitis
Testicular microlithiasis
Cryptorchidism
Testicular Cancer
Secondary Hypogonadism
(Hypogonadotropic
Hypogonadism)
Pituitary Tumors
Pelvic imaging and scrotal
imaging have very limited
roles in the evaluation of
pretesticular causes of
male infertility, which are
usually endocrinopathies,
chromosomal
abnormalities, or chronic
medical conditions
7

8. • A 26 yr old male presented with infertility, breast
enlargement,decreased axillary, pubic hair growth, sparse facial
hair growth,
• On clinical examination small
fi
rm testis noted
• His hormonal work up shows inc.FSH and LH but low
testosterone
• Semen analysis -azoospermia
• Can consider it as Primary hypogonadism (Hypergonadotropic
hypogonadism)
• On USG of scrotum b/l small testis (vol <4ml) noted
• Gynacomastia noted in B/L breast
• Karyotyping revealed 47 XXY (KLIENFELTER SYNDROME)
• On Testicular biopsy
• Many of the tubules exhibit complete hyalinization with
associated hyperplasia of the interstitial cells of Leydig cells
• Note* KLIENFELTER SYNDROME can present at di
ff
erent ages with symptoms speci
fi
c to that age
8

9. • A 20-year-old man presented for evaluation of symptoms of a small-
sized penis and testis(2ml) and poorly developed secondary sexual
characteristics. His birth history revealed that he had been born with a
cleft lip and cleft palate, c/o hyposmia
• His hormonal work up showed
low FSH and LH
• So we can consider as
hypogonadotropic hypogonadism
(Secondary hypogonadism)
• MR images shows
•
The normal anatomy of the region consists of the olfactory bulbs
(blue arrows)
located in the olfactory grooves of the anterior cranial fossa.
The inferior surface of the frontal lobes usually consists of
gyrus rectus (aka straight gyrus) (R) separated from the medial
orbital gyrus (M)
by the olfactory sulcus (yellow arrow). These are absent in
Kallman syndrome.
9

10. • Embryologic failure:
• 1-2,000 gonadotropin neurons (GRH) arise
in the nasal placode and migrate along
olfactory axons to the hypothalamus, in
Kallman, they are stranded at the cribiform
plate"
10

11. A 32 yr old married male patient presented with
decreased libido, secondary infertility,and also
This time his blood work up showed dec. in FSH,
LH, Testosterone, but high levels of prolactin
can be considered as central hypogonadism
And semen analysis showed -oligozoospermia
Next best line of investigation is MRI BRAIN(p+c
Pathophysiology:
Elevated prolactin levels inhibit the normal pulsatile secretion of
gonadotropin-releasing hormone. This leads to a decreased pulsatile
release of follicle-stimulating hormone, luteinizing hormone, and
testosterone and results in spermatogenic arrest and impaired sperm
motility and quality.
Coronal contrast-enhanced T1-weighted
MR image through the pituitary gland
shows a large heterogeneously
enhancing tumor (arrow) consistent with
prolactinproducing macroadenoma.
Prolactinoma
11

12. Testicular causes
VARICOCOELE
• 15% of the general male population.
• 40% in males with primary infertility and
• 81% in males with secondary infertility
• scrotal pain ,discomfort ,
• failed testicular growth and development
• more commonly on the left side or
bilaterally than on the right side alone.
• An isolated right-sided varicocele that
does not decompress while the patient is
supine should raise suspicion for a
retroperitoneal mass, and the patient
should undergo cross-sectional imaging
Grey-scale appearance of varicocele.
Multiple, hypoechoic serpiginous dilated
veins (arrowheads) larger than 3 mm
containing low-level internal echoes
12

13. Sarteschi’s grade I
varicocele. Colour Doppler
images obtained at rest (a)
and during Valsalva (b)
showing dilated veins of
the spermatic cord with
re
fl
ux during Valsalva at
the inguinal canal
Sarteschi’s grade II
varicocele. Colour Doppler
images obtained at rest
(a) and during Valsalva (b)
showing dilated veins in
the supratesticular region
with re
fl
ux during Valsalva
(T=testis)
Sarteschi’s grade III
varicocele. Colour
Doppler images ob9 (a)
and during Valsalva (b)
showing dilated veins to
the inferior pole of the
testis (T) with re
fl
ux
during Valsalva
Sarteschi’s grade IV
varicocele. Colour Doppler
images obtained in supine
position at rest (a) and
while standing during
Valsalva (b). Dilated veins
with re
fl
ux are visible also
at rest. Re
fl
ux increases
while standing during
Valsalva (T=testis)
13

14. Intratesticular Varicocoele
rare and are seen in
fewer than 2% of symptomatic males.
They can occur in isolation or
in conjunction with extratesticular
varicoceles.
Intratesticular varicocele in a 28-year-old man with testicular pain
and infertility. Longitudinal color Doppler US images of the left
testis at rest (a) and during the Valsalva maneuver (b) show tubular
structures with
fl
ow adjacent to the mediastinum testis at rest but
increased dilatation and
fl
ow during the Valsalva maneuver.
Intratesticular varicoceles adjacent to the
mediastinum testis may mimic tubular
ectasia. Tubular ectasia or cystic
transformation of the rete testis—that is,
dilatation of the rete testis—occurs as a
result of partial or complete obstruction of
the e
ff
erent ductules. It is often associated
with spermatoceles and intratesticular cysts.
14

15. • Testicular Atrophy
• Testicular atrophy is considered to be important if the
volume of the affected testis is reduced to 50% of the
volume of the unaffected testis
• This is associated with reduced spermatogenesis and
reduced fertility. It may occur as a result of infarction,
inflammation (epididymo-orchitis), cryptorchidism,
varicocele, trauma, and/or a chronic mass effect.
• Scrotal trauma may lead to ischemia
of viable parenchyma due to
increased intratesticular pressure, and
resorption of nonviable tissue leads to
atrophy and scarring.
• A long-standing extratesticular mass
effect such as that resulting from a
hydrocele may compromise testicular
blood flow and result in atrophy.
• Testicular size discrepancy is two
times more common in infertile males
with varicoceles than in those without
varicoceles.
• Liver cirrhosis, estrogen treatment,
and hypopituitary disorders also may
cause testicular atrophy.
15

16. • Testicular torsion
• twisting of the spermatic cord that results in progressive
impairment of venous drainage and ultimately arterial
ischemia.
• one of the leading causes of acute scrotal pain and male-
factor infertility,when left untreated.
• The ischemic changes of the testis depend on the duration
and degree of rotation, which can range from 180° to 720°.
• Ischemia and reperfusion injuries result in germ cell
apoptosis, testicular atrophy, and loss of spermatogenesis,
usually 6 hours after the onset of torsion. After 12 hours, the
testis loses its Leydig cell function.
• Detorsion within 4–6 hours of the acute onset has proven to
be successful in salvaging a torsed testis in more than 90%
of cases . Testicular torsions usually occur in the medial
direction. Manual detorsion should be attempted away from
the midline, and the disappearance of pain is considered a
sign of a successful maneuver.
16

17. Ultrasound of the testes demonstrates the right testis to be enlarged,
heterogeneous in echotexture, and without evidence of any blood
fl
ow. Features are consistent with testicular torsion.
the whirlpool sign refers to a lamellated
mass with concentric layering just cephalad
to the testis representing the coiled
spermatic cord components
• Initially, torsion is su
ffi
cient only to
obstruct venous out
fl
ow (incomplete
torsion, less than 360 degrees),
resulting in the gradual increase in
intratesticular pressure and
resistance.
• altered blood
fl
ow
in incomplete torsion
elevated resistive index (RI >0.75)
17

18. • Orchitis and Epididymo-orchitis
• Epididymoorchitis in a 25-year-old man
who reported having testicular pain during
infertility workup.
• heterogeneous enlargement of the right
testis (dashed arrow in b) and epididymis
(solid arrow in b), with increased flow in
both structures compatible with
hyperemia.
• Scarring secondary to infection and
in
fl
ammation may lead to
obstructive azoospermia.
• Chronic epididymitis and
epididymo-orchitis can result in
testicular atrophy.
• Pure orchitis is uncommon and
most often results from the mumps
18

19. • Granulomatous epididymo-orchitis seen in a 40-year-old man during infertility
workup. multiple small hypoechoic nodules (solid arrows) di
ff
usely scattered
throughout the left testis in a miliary pattern.
• The head and tail of the epididymis are nodular, with inhomogeneous
hypoechogenicity (* in a), consistent with tubercular epididymo-orchitis. Mild
scrotal thickening (dashed arrow) and a hydrocele also are present.
• Chronic in
fl
ammation can occur as a result of granulomatous processes such
as tuberculosis, syphilis, sarcoidosis, and other causes
19

20. Testicular Microlithiasis
• Testicular microlithiasis is a rare condition
that is present in 0.6%–9.0% of males with
symptoms and in 2.4%–5.6% of adults
without symptoms who are referred for US
• The presence of testicular microlithiasis
has been associated with infertility,
cryptorchidism, testicular atrophy,
Klinefelter syndrome, hypogonadism,
pseudohermaphroditism, and alveolar
microlithiasis
• Twenty to 60 percent of the seminiferous
tubules are usually involved, with the
resultant oligospermia and reduced sperm
motility possibly explaining the association
of testicular microlithiasis with infertility
26-year-old man who presented to the infertility
clinic with abnormal semen analysis results.
Longitudinal color Doppler US image of the left
testis shows innumerable(>5) tiny(<3mm) echogenic,
nonshadowing foci in the testicular parenchyma,
consistent with classic testicular microlithiasis.
20

21. A 30-year-old man having a left testicular
mass at infertility workup. heterogeneous
lobulated mass with increased vascularity,
consistent with a seminoma, in the left testis.
Testicular Cancer.—
Testicular Cancer • Patients who have testicular tumors at
presentation often have reduced semen
quality and fertility, as the function of
both the a
ff
ected testis and the
una
ff
ected testis is impaired at the time
of diagnosis.
• This impairment may be due to multiple
factors, including disruption in the
hypothalamic-pituitary-gonadal axis,
immunologic or cytologic injury to the
germinal epithelium, systemic cancer–
related processes (eg, fever and
malnutrition), and psychological
conditions such as anxiety and
depression
21

22. • Post testicular causes
• When physical examination and
semen results are normal, obstruction
of the ductal system, which accounts
for up to 40% of azoospermia cases,
should be suspected .
Epididymal Obstruction Vas deferens obstruction
M/c-Gonococcal and chlamydia
infection-scarring-obstruction
M/c -Post vasectomy
Surgical removal of epididymal cysts
(ie, spermatocelectomy) and trauma
inguinal hernia repair, improperly
performed vasography, or contrast
medium–induced irritation
Congenital conditions
1. ductal atresia,
2. stenosis,
3. prostatic cysts,
4. ejaculatory duct cysts,
5. seminal vesicle cysts
can result in ejaculatory
duct obstruction
Acquired conditions
infection,
1. scarring due to previous
surgical procedures (ie, bladder
neck repair),
2. prolonged catheterization,
in
fl
ammation,
3. and stone formation in the
distal duct at the level of the
ampulla may lead to proximal
duct dilatation
Ejaculatory Duct Obstruction
• In most males, infertility is the
fi
rst
symptom of ejaculatory duct
obstruction
• other symptoms include decreased
ejaculatory force,
• pain during ejaculation,
• hematospermia,
• perineal or testicular pain, and
prostatitis-like symptoms.
• Semen analysis usually reveals low
semen volume, low semen pH, and
absent fructose
22

23. Epididymal tubular ectasia in a 40-year-old man who
underwent a vasectomy 15 years earlier and was interested
in vasectomy reversal. Longitudinal gray-scale US images
through the head (a) and tail (b) of the right epididymis show
tubular structures with obstruction-induced dilatation
(arrow) involving the right epididymis, consistent with
tubular ectasia of the epididymis.
23

24. Cystic Lesions
24

25. Congenital bilateral absence of the vas deferens
• the most common cause of extratesticular ductal system obstruction;
• Agenesis of the vas deferens can be unilateral or bilateral and partial or complete,
and it can be associated with hypoplasia of the epididymis.
• Embryologically, the vas deferens arises from the wolffian duct at week 7 of
gestation; therefore, aplasia of the vas deferens can occur as a result of fetal insult.
• Cystic fibrosis, a well-known cause of congenital bilateral or unilateral absence of
the vas deferens, is an autosomal recessive disease in which the genetic mutation
of the cystic fibrosis transmembrane conductance regulator (CFTR) gene located
on the short arm of chromosome 7 causes secondary atresia of one or both vas
deferentia during embryogenesis
• Findings in CBAVD due to cystic fibrosis include agenesis of the vas deferens,
hypoplastic or nonfunctioning seminal vesicles and ejaculatory ducts, and an
epididymal remnant composed of a firm and distended caput region
Spermatogenesis is not impaired in these patients, and sperm may be harvested
from the epididymis.
25

26. Erectile dysfunction
• main role of imaging in the setting of erectile dysfunction is to
differentiate between vascular and nonvascular causes of erectile
dysfunction, and penile Doppler US is the modality of choice for this
evaluation
• In whom arterial or venous insufficiency is suspected and there is little
or no functional response to phosphodiesterase-5 inhibitor agents.
• The peak systolic velocity is considered normal if it is greater than 35
cm/sec, and the end-diastolic velocity is usually normal if it is a
negative value or close to 0 cm/sec.
• A peak systolic velocity of less than 25 cm/sec indicates severe
arterial disease
• An end-diastolic velocity greater than 5 cm/sec suggests failed
cavernosal engorgement and venous incompetence, which manifest
as persistent diastolic flow. An end-diastolic velocity of 5–7 cm/sec is
diagnostic for venous incompetency
26

27. 1)corpora cavernosa
2)corpus spongiosum, 3)tunica albuginea
,4) cavernosal artery, 5) helicine arteries
1
3
5
27

28. 28

29. Post papaverine
injection
§minutes
10minutes
15 minutes
20 minutes
25 minutes
PRE & POST papaverine
injection 60 mg of papaverine (2
mL ampoule of 30 mg/mL)
5minutes
10minutes
15 minutes
20 minutes
25 minutes
Cavernosal artery (both left
and left artery )
1. Diametre is (0.6-1.0 mm),
2. PSV
3.EDV
4.RI
29

30. • Peak systolic velocity is the
best Doppler indicator of
arteriogenic impotence.
• PSV >30 cm/sec -Normal
• PSV 25-30 cm/sec -not
speci
fi
c
• PSV <25 cm/sec - arterial
dysfunction.
• A di
ff
erence of greater than
10 cm/s between the PSV
of both cavernosal arteries
suggests arteriogenic ED
• End-diastolic velocity is
the best Doppler indicator
of venogenic impotence.
• EDV <5cm/sec is normal
• EDV>5 cm/sec indicates
venous dysfunction, failed
cavernosal engorgement
and venous incompetence,
which manifest as
persistent diastolic
fl
ow.
• A good diastolic reversal
virtually rules out venous
insu
ffi
ciency.
Elevated EDV usually
involves a decrease
in the RI;
hence, an RI of less
than 0.80 is
indicative of
inadequate corpora
blood retention (i.e.,
venous dysfunction)
RI >0.8
30

31. PSV <25 cm/s at all intervals
and low-resistance spectral
waveforms, compatible with
arterial insu
ffi
ciency.
PSV > 30 cm/s) with EDV> 5 cm/s
and RI <0.75, suggestive of venous
incompetence.
31

32. CONCLUSION
• The diagnostic workup of male infertility should be
systematic and structured; however, it should not be
started before the infertile couple has attempted to
achieve pregnancy for 1 year.
• Imaging has an important role in differentiating causes of
obstructive azoospermia, which are potentially correctable
causes of infertility, from causes of nonobstructive
azoospermia. It is also critical to rule out the presence of
life-threatening conditions associated with infertility and
genetic conditions that can be transmitted to offspring.
32

33. FEMALE INFERTILITY
33

34. FALLOPIAN TUBE ABNORMALITIES
HSG provides optimal depiction of the fallopian tubes, allowing detection
of tubal patency, tubal occlusion, tubal irregularity, and peritubal disease.
34

35. M/c causes
1.Tubal spasm
2.Infection
3.Prior surgery
Rare causes
1.granulomatous salpingitis due to
tuberculosis,
2. intraluminal endometriosis,
3.parasitic
infection,
4. congenital atresia of the fallopian
tubes
Tubal Occlusion
35

36. • occlusion at the ampullary end of the fallopian
tube, a condition most commonly caused by
pelvic in
fl
ammatory disease.
absence of
contrast material
out
fl
ow
• important to prescribe
postprocedural antibiotic
prophylaxis, typically
doxycycline, to prevent
procedure-related infection
due to stasis of contrast
material within the obstructed
fallopian tube
• Treatment of distal tubal
occlusion may include
fl
uoroscopically guided
transcervical fallopian tube
recanalization; however, tubal
microsurgery may be
performed if recanalization is
not successful
Hydrosalpinx
36

37. Tubal Irregularity
• salpingitis isthmica nodosa,an inflammatory
process within the fallopian tube.
• The exact cause of this process is unknown,
but associations with pelvic infl ammatory
disease, infertility, and ectopic pregnancy
have been reported
• Because tubes affected by this disease are
not readily amenable to recanalization,
patients typically are offered in vitro
fertilization.
• Spot (a) and magnified (b) views from HSG depict
multiple contrast material–filled luminal pouches
(arrowheads) projecting 2–3 mm outward from the
isthmic portion of both fallopian tubes.
37

38. • Peritubal Abnormalities
• Even when the fallopian tubes appear normal,
an abnormal accumulation of contrast
material may be seen adjacent to the
ampullary ends of the tubes at HSG.
Right peritubal pelvic adhesion due to previous pelvic in
fl
ammatory disease. Early (a) and late (b) HSG show
normal contrast material
fi
lling of the right fallopian tube (arrow in a) and a rounded collection of leaked
contrast material (arrowheads in b) adjacent to the ampullary portion of the right tube. The collection was due
to peritubal adhesions. The left fallopian tube appears normal and patent.
• Both endometriosis and
pelvic in
fl
ammatory
disease may lead to
peritubal adhesions with
resultant infertility.
• When evidence of
peritubal adhesions is
seen at HSG, pelvic MRI
is particularly helpful for
further noninvasive
evaluation.
38

39. • ENDOMETRIOSIS (by the presence of
endometrial glands and stroma outside the
uterus )
• This condition almost exclusively affects
women during their reproductive years. It
may be asymptomatic or may cause
multiple symptoms, including pelvic pain
and infertility.
• Endometriosis may take the form of either
small implants or cysts that change in size
and appearance during the menstrual cycle
and that may initiate an inflammatory
response leading to fibrosis and adhesions.
• Endometriotic cysts, referred to as
endometriomas, result from repeated
hemorrhage within an implant.
US has low sensitivity for the detection of focal
implants, but it may depict endometriomas
Sagittal transvaginal US image obtained in a
woman with a history of endometriosis shows
an ovarian mass with multiple faint internal
echoes (arrows) and several hyperechoic
mural foci (arrowheads).
They generally occur within the ovary, often
bilaterally.
39

40. The symptoms depend on the
localization of the endometriosis,
the depth of the in
fi
ltration and
whether the endometriosis is
complicated by adhesions.
• ovarian endometrioma
• retrocervical endometriosis
• deep bowel endometriosis
• bladder endometriosis
• abdominal wall endometriosis
• small solid deep lesions
may be hyperintense on T1 and hypointense on T2
• adhesions and
fi
brosis
1. isointense to pelvic muscle on both T1 and T2
weighted images
2. spiculated low signal intensity stranding that
obscures organ interfaces 1
3. distortion of normal anatomy
• posterior displacement of the uterus
• kissing ovaries sign: seen in the severe forms of
the disease
• angulation of bowel loops
• elevation of the posterior vaginal fornix
• Loculated
fl
uid collections, hydrosalpinx
Note*
• However, the sensitivity (13%) of MR imaging for the detection of endometrial implants is
low,for this reason, MR imaging alone cannot take the place of laparoscopy for the de
fi
nitive
diagnosis of endometriosis
40

41. • Lesions usually demonstrate low to
intermediate signal intensity on T2- and T1-
weighted images.
• In some cases punctate foci of high signal
intensity are seen on T2-weighted imaging,
indicating dilated endometrial glands.
Foci of high signal intensity may be seen on
T1-weighted images.
• If these foci also have a high signal intensity
on T1-weighted images with fat saturation, it
indicates the presence of hemorrhage.
• T1-weighted images with fat saturation are
necessary to di
ff
erentiate blood in
endometriomas from fat in mature cystic
teratomas, since both show high signal
intensity on T1-weighted images without
fatsat.
Unenhanced axial T1weighted fat-
suppressed MR image shows dilatation of the
right fallopian tube (arrow) with internal high
signal intensity due to blood products,
fi
ndings indicative of hematosalpinx. Smaller
high-signal-intensity foci along the posterior
uterine serosa (arrowhead) are indicative of
endometrial implants.
41

42. • INTRAUTERINE FILLING DEFECTS
air bubbles in the contrast material injection,
• *NOTE-most of the times
fi
lling defects caused byair bubbles in the contrast
material injection,
• Bilateral oblique views may help identify mobile, nondependent, round
fi
lling
defects caused by air bubbles and to avoid mistaking these
fi
ndings for
intrauterine disease.
Blood clot
• More contrast material may be injected into the endometrial cavity to see whether the
fi
lling defects move; for example, the additional injection may cause air bubbles to be
ejected via the fallopian tubes . Early views of the uterus should be obtained at HSG
because small
fi
lling defects may become obscured with more advanced opaci
fi
cation
of the endometrial cavity
42

43. Asherman syndrome (infertility 2* to
synechiae) in a patient with a history of
dilation and curettage. (a) HSG depicts
several linear intrauterine
fi
lling defects
(arrowheads). (b) Sagittal image from
hysterographic TVS shows echo genie
bands that traverse the endometrial cavity
(arrows).
• result of previous pregnancy, dilation and curettage, surgery,
or infection.
Uterine Synechiae(Intrauterine adhesions)
• irregular linear
fi
lling defects and in addition theendometrial cavity may appear
distorted or may not expand as expected with the injection of contrast material.
• To accurately diagnose the condition, uterine adhesions must be di
ff
erentiated from
normal uterine folds, which also may appear as longitudinal
fi
lling defects when the
endometrial cavity is not fully distended
43

44. • Even subcentimetric endometrial
polyps and submucosal leiomyomas
may interfere with embryo transfer
and implantation .
• Hysterographic US can depict
endometrial lesions that are not visible
with pelvic US and can help
distinguish endometrial polyps from
submucosal leiomyomas.
• It also allows a more accurate
assessment of the number and
location of endocavitary lesions, thus
providing guidance for their
subsequent management with
hysteroscopic biopsy or excision.
Endometrial Polyps
Endometrial polyp. (a) HSG depicts a well-
circumscribed ovoid intrauterine
fi
lling
defect (arrow). Sagittal gray-scale US
images from subsequent transvaginal
hysterographic US show a posterior fundal
endometrial polyp (arrowheads in b) with a
central feeding vessel (arrow in c).
44

45. Endocavitary leiomyoma (
fi
broid). Sag TVS (a) and color
Doppler (b) US images depict a solid mass
(arrowheads) with internal echogenicity similar to that
of the myometrium. The mass has a pedunculated
attachment (arrow) to the uterus and extends into the
cervical canal.
Submucosal leiomyomas typically appear as
hypoechoic masses that distort the normal
appearing endometrium on US images
They may have a peduncular attachment and thus
mimic an endometrial polyp
A leiomyoma with more than 50% of its volume
within the endometrial cavity may be treated
e
ff
ectively with hysteroscopic myomectomy
Submucosal Leiomyomas
45

46. UTERINE CONTOUR IRREGULARITIES
• Adenomyosis
• a benign pathologic condition of the
uterus, is characterized by the presence
of ectopic endometrial glands within the
myometrium, with surrounding smooth-
muscle hyperplasia
• di
ff
usely or may occur as a focal
lesion (adenomyoma)
• may be associated with infertility due to
impaired uterine contractility, which is
necessary for directed sperm transport
through the uterus
• Focal adenomyomas, especially in
submucosal locations, also may impair
fertility.
HSG shows characteristic linear or saccular
contrast material collections (arrowheads)
protruding beyond the normal contour of the
endometrial cavity.
46

47. Adenomyosis. Sag TVS shows globular
uterine enlargement with asymmetric
thickening and heterogeneity of the
myometrium (arrows) and poor de
fi
nition
of the endomyometrial junction
(arrowheads). Myometrial cysts can also
been sometimes
Sagittal T2-weighted MR image shows high-signal-
intensity foci (arrow) indicative of ectopic endometrial
glandular implants with associated thickening of the
junctional zone (> 12 mm) (arrowheads) due to
smooth-muscle hypertrophy in a patient with focal
anterior body adenomyosis. . A junctional zone
thickness of less than 8 mm virtually excludes the
diagnosis, whereas a thickness of 8–12 mm requires
additional investigation.
47

48. • Leiomyomas
Submucosal leiomyomas.HSG
shows a large intrauterine
fi
lling
defect, due to a large submucosal
leiomyoma(arrows) that produces a
mass effect on almost the entire
uterus.
Axial T2-weighted MRI demonstrates a
region of heterogeneous increased signal
intensity that represents a fundal
intramural
fi
broid (arrow) with a
submucosal component (arrowheads).
Nabothian cysts are visible in the cervix.
48

49. They may be largely submucosal and distort the
endometrium, or they may occur as discrete intracavitary
mass lesions( Endocavitary leiomyoma) Sagittal transvaginal
US image depicts a well-circumscribed hypoechoic mass
(arrow) centered within the endometrium (E), with a posterior
acoustic shadow extending from the edges of the mass. An
endocavitary leiomyoma was resected at hysteroscopy.
Endocavitary leiomyoma. Sagittal T2W MR
image shows a mixed-signal-intensity
heterogeneous mass (arrows) within and
distending the endometrial cavity, a
fi
nding
characteristic of an endocavitary leiomyoma.
Several intramural
fi
broids (arrowheads) also
are visible.
49

50. Cervical Abnormalities
• Cervical Stenosis
• clinically defined as cervical narrowing that prevents the insertion of a 2.5-mm-
wide dilator.
• This condition may be congenital or secondary to infection or trauma.
• Risk factors include previous cone biopsy, cryotherapy, laser treatment, and
biopsy for cervical dysplasia.
• The more severe the stenosis, the more likely it is to be symptomatic
• Consequences of cervical stenosis include obstruction of menstrual flow with
resulting amenorrhea, dysmenorrhea, and potential infertility due to inability of
sperm to enter the upper genital tract Cervical stenosis also may be a serious
impediment to assisted fertility techniques including embryo transfer and
intrauterine insemination
50

51. • At HSG, cervical stenosis may appear as
narrowing of the endocervical canal
(normal diameter, 0.5–3.0 cm), or it may
manifest as complete obliteration of the
cervical os, preventing insertion of the
HSG catheter
• Observations of narrowing of the
endocervical canal on HSG should be
correlated with clinical findings, because
the diameter of the normal endocervical
canal and internal os may vary
• At US, hematometra manifests as
dilatation of the
fl
uid-
fi
lled endometrial
cavity, often with a
fl
uid-
fl
uid level
caused by sedimentation of red blood
cells.
• Masses such as cervical polyps,
fibroids, and neoplasms also
may cause narrowing of the
cervical lumen.
• Gradual dilation of the cervix,
performed with US guidance, is
an effective treatment for this
problem
51

52. • Ovarian Abnormalities
• Ovarian causes of infertility include primary conditions such as
nonfunctional ovaries, premature ovarian failure, and absence of
ovaries (gonadal dysgenesis).
• These conditions are usually diagnosed on the basis of clinical
and biochemical findings.
• Imaging is more valuable for diagnosing the secondary ovarian
causes of infertility, which include polycystic ovary syndrome,
endometriosis, and ovarian cancer.
• Pelvic US is usually performed for initial evaluation of the ovaries.
52

53. PCOS
Morphologic alterations that may be detected
at pelvic in more than 80% of women with a
clinical diagnosis of polycystic ovary
syndrome
include enlarged ovaries,
increased echogenicity of the ovarian
stroma,
increased number of small follicular-type
cysts (a
fi
nding of at least 12 cysts was
proved diagnostically speci
fi
c but not
sensitive)
53

54. • NOTE****
• Just finding of polycystic ovaries at US is not diagnostic for the syndrome,
because 20%–30% of the normal population, particularly young women, may
have ovaries with this appearance.
• Polycystic ovary syndrome is a functional disorder: Polycystic ovaries need not
be present for the diagnosis to be made; and conversely, in the absence of other
signs and symptoms, their presence is not sufficient to establish the diagnosis.
• In some patients with polycystic ovary syndrome the ovaries are enlarged, but
the range of sizes of diseased ovaries overlaps widely with that of normal
ovaries.
• Increased echogenicity of the ovarian stroma is the most sensitive and specifi c
US sign of the syndrome, but the finding is subjective. At MR imaging, the
ovaries in patients with polycystic ovary syndrome classically demonstrate a low-
signal-intensity central stroma surrounded by small peripheral cysts on T2W
images
54

55. 1. enlarged size of the ovary ≥ 10 cc
2. increased number of follicles per
ovary (FNPO) atleast 12 to 20
3. peripherally arranged follicles
'String of pearls sign'
4. echogenic central stroma
5. small-sized follicles 2-9 mm
Coronal T2-weighted MR image
from the same patient shows
bilateral ovarian enlargement
with multiple peripheral follicles
(arrows).
55

56. • FOLLICULAR MONITORING
• Journey to ovulation begins during late luteal phase of prior menstrual cycle,
when certain 2-5 mm sized healthy follicles noted in ovary, from which
dominant follicles is to be selected for next cycle This process is called
'recruitment'.
• Usual number of such follicles may be 3-11, which goes on decreasing with
advancing age 1.
• During Day 1-5 of the menstrual cycle, a second process of 'follicular
selection' begins, when among all recruited follicles, certain growing follicles of
size 5-10 mm are selected, while rest of the follicles regress or become atretic.
• During Day 5-7 of the menstrual cycle, a process of 'dominance' begins, when
a certain follicle of 10 mm size takes the control and becomes dominant.
• This also suppresses the growth of the rest of the selected follicles, and in a
way, is destined to ovulate.
• This follicle starts growing at rate of 2-3 mm a day and reaches 17-27 mm size
just prior to ovulation.
56

57. • One important learning point in this regard is, "largest follicle on
day 3 of the cycle, may or may not be a dominant follicle in the
end.
• Process of dominance begins late, when suddenly a certain
underdog follicle starts growing faster and suppresses others to
become dominant".
• Almost nearing ovulation, rapid follicle growth takes place, and
follicle starts protruding from the ovarian cortex, attains a
crenated border, and it literally explodes to release the ovum,
along with some antral
fl
uid.
57

58. Once the follicle reaches 16 mm size, a daily monitoring of
follicle is recommended.
Next step is documentation of ovulation. Ovulation is
sonographically determined by the following sonographic signs:
• follicle suddenly disappears or regresses in size
• irregular margins
• intra-follicular echoes. Follicle suddenly becomes more
echogenic
• free fluid in the pouch of Douglas
• increased perifollicular blood flow velocities, on doppler
58

59. • Most of the IVF studies are conducted after induction of ovaries with help of ovulation
inducing agents like Clomiphene citrate. In such induced cycle, primary determinants
of success are:
• Ovarian volume is easy to measure, although not a good predictor of IVF outcome.
Now, it is documented, that a low ovarian volume does not always lead to
anovulatory cycle. But, it is important to recognize a polycystic ovarian pattern and
di
ff
erentiate it from post-induction multicystic ovaries. While, follicles in the center as
well as the periphery, are seen in normal induced multicystic ovaries 4.
• Antral follicle number of less than three 5, usually signify possible failure of assisted
reproductive therapy (ART).
• Ovarian stromal blood
fl
ow a good predictor of ART success. Increased peak systolic
velocity (>10 cm/sec) is one of such parameters which has been advocated.
59

60. • European classi
fi
cation system ESHRE/ESGE from
2013.
• Class U0 is a normal uterus
• Class U1 is a dysmorphic shaped uterus either as a T-
shaped cavum due to abnormally thick uterine walls
or as a T-shaped cavum due to an abnormal outer
contour (infantilis).
• Class U2 is the result of failure of resorption of the
septum. There is an internal indentation. The outer
contour of the uterus is normal and this differentiates
the septate uterus from the bicorporeal uterus.
• Class U3 is a bicorporeal uterus with a left and right
corpus as a result of failure of fusion. The outer
contour is abnormal with an external cleft of the
fundus. A bicorporeal septate uterus has both an
external cleft and a septum.
• Class U4 is a hemi-uterus as a result of unilateral
failure of formation of the Müllerian duct.
• Class U5 is an aplastic uterus as a result of bilateral
failure of formation of the Müllerian ducts.
• Class U6 are unclassi
fi
ed cases
Müllerian Duct Anomalies
60

61. CHECKLIST
1. Presence of uterus
Is there a uterus or is there a hemi-
uterus U4 or uterus aplasia U5.
2. Fundal external contour
Is there an external indentation of more
than 50% of the uterine wall thickness
(UWT) as in bicorporeal uterus U3.
3. Internal indentation in uterine cavity
Is there an internal indentation of more
than 50% of the uterine wall thickness
as in septate uterus U2.
4. Kidneys
Are there renal anomalies?
5. Cervix and vagina (co-existent
classes)
61

62. MULLERIAN DUCT ANOMALIES Congenital malformation of uterus.
A: The unicornuate uterus with a
single fallopian tube.
B: Didelphys uterus, two separate
uterine cavities and two separate
endocervical canals.
C: The bicornuate uterus (angle
formed by the medial borders of two
hemicavities >105°)
D: A septated uterus (angle formed
by the medial borders of two
hemicavities <60°).
E: The arcuate uterine.
F: Appearance of a DES-exposed
woman in HSG. HSG shows a T-
shaped uterus with an irregular
endometrial contour and a very long
endocervical canal.
62

63. 63

64. THANK YOU
64