Case Study

CASE STUDY-UTERINE FIBROID/LEIOMYOMA IN PREGNANCY
INTRODUCTION
Uterine fibroids or leiomyomas represent benign hormone-dependent tumours of

smooth muscle on the uterine wall, occurring in 20–60% of women of reproductive
age and are a very common finding in premenopausal women, Pavone, D. et
al (2018). The development of fibroids is related to various risk factors, such as age,
race, hormonal factors, uterine infection, obesity and behavioural factors, but the
epidemiological data are inconsistent. Generally, as postulated by Parker, W.H
(2007), they are asymptomatic, and only about 30% of these fibroids are large enough
to be discovered by a health care practitioner during a physical examination. In
addition, approximately one-third of them develop serious clinical manifestations,
such as abnormal uterine bleeding, anaemia, back pain, pelvic pain and pressure,
constipation, urinary frequency or infertility, thus necessitating treatment.
Moreover, scientific data reports that fibroids have been linked to poor obstetric
outcomes, are found in 0.1–10.7% of pregnant women, and their prevalence rises if
women want to postpone having children until a later age. Pregnancy-related
hormones influence the size of uterine fibroids, and fibroids have many impacts on
pregnancy. Women with uterine fibroids in pregnancy generally have concerns related
to adverse outcomes. However, these women generally have uneventful outcomes in
pregnancy. Several studies have reported inconsistent relationships between uterine
fibroids and adverse obstetric outcomes. Miscarriage, premature labour, antepartum
haemorrhaging, malposition, malpresentation, obstructed labour, uterine inversion,
post-partum haemorrhaging and puerperal sepsis are among the obstetric
consequences of co-existing uterine fibroids in pregnancy.
It is known that uterine fibroids, especially multiple, intramural or sub-mucosal, are

associated with an increased risk of early pregnancy loss. Fibroids developed in the
uterine body are more likely to cause miscarriage than fibroids in the lower uterine
area. Enhanced uterine irritability and contractility are suggested factors that lead to
increased pregnancy loss when there is a co-existing fibroid (Klatsky, P.C. et al
2008), a compressive effect and a disruption of blood flow to the placenta and foetus.
This is more likely when the placenta implants close to a fibroid nodule, and this
depends on the location of the uterine fibroids. The pregnant patient in this case
presented to the radiology department with a history of abdominal pain, vaginal
bleeding, abdominal heaviness, nausea, vomiting and loss of appetite.
INDICATION
Lower abdominal pain and vaginal bleeding in pregnancy. ??? cause and foetal well
being.
EXAMINATION DATE
PATIENT INFORMATION
Date of Birth 22 March 1980
Parity 0
Gravida 1
Last Menstrual Period 27 May 2022
Contraceptive Nil
Marital Status Married
Sex Female
Level of Education Ordinary Level
EQUIPMENT
 Mindray DC-6 Ultrasound machine.
 3.5-5MHz curvilinear probe .
 Sony High glossy thermal paper.
 Ultrasound gel.
 Sony Ultrasound Printer.
PATIENT PREPARATION, PATIENT CARE AND PROTOCOL

Standard second trimester pregnancy transabdominal scan protocol documented in
appendix A attached
OBSERVATIONS AND FINDINGS
 A bulky gravid uterus was seen with a well-defined echogenic ring surrounding
an anechoic centre located centrally. The gestational sac had anechoic contents
embedding an echogenic embryo. The gestational sac occupies approximately
one-half of the uterine volume.
 A live embryo was seen lying horizontally in the gestational sac. Pulsations were
seen on the embryo resembling an embryonic heart motion and M-mode was used
to measure the heart rate.
 A yolk sac was not visualised.
 There were some high level echoes seen appearing as a group of echoes in a
crescentic shape in a subchorionic location, or between the gestational sac and the
decidual reaction.
 The cervix was relatively long and closed measuring 5.57 cm long and no
echogenic or hypoechoic signs of bleeding was seen in the cervix.
 Two anterior and posterior myometrial inhomogeneous, hypoechoic and well
defined subserosal masses solid masses were seen. The larger fundally located
mass measured 4.03 cm x 2.82 cm whilst the smaller one measured 1.76 cm x
1.57 cm.
 Both ovaries were not one in the uterine fundus and the other posterior to the
gestational sac visualised during scanning. No adnexal solid or cystic masses
were seen.
 There was no free fluid collection seen in the pouch of Douglas.
 The urinary bladder was distended with a smooth mucosal outline and anechoic
contents. There was no sonographic evidence of urinary bladder wall thickening,
urinary bladder calculi or wall masses seen.
Foetal Biometry And Dates
Serial Parameter Measurement (cm) Corresponding EGA
(a) (b) (c) (d)

1. GS 3.04 7 Weeks 4 Days
2. CRL 1.56 8 Weeks 0 Days
Uterine Measurements
Serial Parameter Measurement (cm)
(a) (b) (c)
1. Uterine length 11.56
2. Uterine width 9.22
3. Uterine height 7.18
4. Uterine volume 400.3 cc
5. Uterine body 27.96
6. Cervix length 5.57
 Therefore the average EGA was 7 weeks 5 days

 The assigned EDD by scan was 10 march 2023 +/-2 days
Comment
1. Single live intrauterine embryo of 7 weeks 5 days gestational age by scan.
2. Perisac/ subchorionic bleeds ??? (Extra gestational bleeds).
3. The anterior and posterior myometrial inhomogeneous hypoechoic well
defined masses measuring 4.03 cm x 2.82 and 1.76 cm x 1.57 cm respectively are
suggestive of subserosal fibroids (Fibroids in Pregnancy).
4. Recommend a follow-up sonogram in one or two week to assess pregnancy
progression.
5. Correlate clinically.
Signed………………………………….S. TANGWADZANA
(Diagnostic Radiographer/Student Sonographer)
DISCUSSION
Etiology and Pathophysiology
Although, the exact etiology of fibroid is not known yet, the growth of uterine fibroid
is featured as a benign, hormone sensitive diffuse or nodulus hyperplasia of
myometrium, and is characterized by having multiple factors of pathogenesis and
systemic changes. Uterine fibroid is developed on the background of hyperestrogens,
progesterone deficits and hypergonadotropins. The majority of the researchers
consider that the growth of fibroid depends on concentration of cytosolic receptors to
the sexual hormones and their interactions with the endogenous or exogenous
hormones. In accordance to clinical observations, it can be admitted that both growth
and regression of fibroid are oestrogen-dependant; the tumour size gets increased
during pregnancy and is regressed after menopause.
Uterine Fibroid And Pregnancy

Effects of Pregnancy
The most frequent benign uterine tumour is leiomyoma/fibroma/fibroid which
originates from the uterine smooth muscle tissue (myometrium) whose growth is
dependent on progesterone and oestrogen. Normal rapid uterine expansion that occurs
during pregnancy is likely a more complex mechanism mediated in part by oestrogen,
progesterone, various growth factors especially platelet-derived growth factor and an
increase in cells with Ki-67 antigen, (Kurjak,. A and Chervenak,. F. A. 2011).
These observations support the concept that the same or similar hormonal and growth
factors that normally cause uterine growth during pregnancy also stimulate growth of
fibroid early in pregnancy. This may serve to explain the paradoxical observations
that large fibroids remain unchanged or increase in size late in pregnancy. It is likely
that during pregnancy, fibroid oestrogen receptors are down regulated due to massive
amounts of oestrogen. Without effective oestrogen receptors and thus oestrogen
action in the fibroids, epidermal growth factor binding is also decreased.
These fibroids frequently cause abnormal menstrual periods, pelvic pain, and pressure
symptoms on nearby tissues and organs. When the urinary bladder, ureters, and other
nearby organs are subjected to pressure, they can be lethal in some situations. (14)
The actual cause of uterine fibroids has yet to be determined. However, cytogenetic
and genetic investigations indicate that they are caused by somatic mutations in
myometrial cells with chromosome 6, 7, 12, and 14 abnormalities.
Possible Causes of Fibroids

Genetics: About 40% of fibroids contain alterations in genes that code for uterine
muscle cells. Patients with hereditary leiomyomatosis and renal cell carcinoma
(HLRCC cutaneous and uterine leiomyoma) are at risk for papillary renal cell
carcinoma (the incidence in women is greater than in men). They also have mutation
in fumarate hydratase gene. The chromosomal anomaly (12q13–15) is quite common
in myomatous cells. In fact, in 30–40% cases, the predisposition to uterine fibroid is
passed down from mothers to daughters on hereditary line. A form of fibroid so called
“family type” is present where uterine fibroid are seen in all the family line, i.e. in
grandmother, mother, aunts and sisters.
Heredity: If a mother or sister had fibroids, then there is an increased risk of
developing them.
Race: Black women are more likely to have fibroids than are women of other racial
groups. Also, black women have fibroids at younger age and they are more likely to
have more or larger fibroids.
Hormonal imbalance: Oestrogen and progesterone appear to promote the growth of
fibroids. Fibroids contain more oestrogen and oestrogen receptors than do normal
uterine muscle cells. Other chemicals that help the body maintain tissues, such as
insulin-like growth factor, may also affect fibroid growth.
Obesity: Overweight women have a greater risk of developing fibroids. Fibroids
rarely have malignant potential (leiomyosarcoma).
Pregnant patients with fibroids are exposed to a high rate of complications during
antepartum, intrapartum, and postpartum periods. The prevalence of uterine fibroids
during pregnancy reported in some studies ranges from 1.6 to 16.7%, varying from
one trimester to another, (Shavell, V.I. et al, 2012). Previous data show that the
number of fibroids increases with the patient’s age. Like the literature data, which
indicate that fibroid distribution in pregnant women increases beyond the age of 35,
the patient’s age in this case is 42 years, of black race and nulliparity. It seems that
nulliparity plays an important role in the etiology of fibroids. It is known that
circulating hormones, such as oestrogen and progesterone, are considered modulators
for tumour growth. Consequently, fibroids should develop more frequently in
pregnancy. Being of the black race, nulliparity, and being of reproductive age are all
risk factors in this patient.
The presence of fibroids in very young women can be correlated with a strong family
history, but in this case the patient had mentioned having a negative first-degree
relative with uterine fibroids and neither had she knew of anyone with fibroids in her
hereditary collateral history. Adipose tissue is a recognized extra source of oestrogen,
which is thought to play a role in the development of fibroids. The prevalence of
overweight and obesity is on the rise, being higher in urban area and among educated
women. However, in the present case study, the patient is not obese.
In this case study, diagnoses was made in the first trimester. This can be explained by
the fact that more and more pregnant women are going to the gynaecologist to
evaluate pregnancies from the first trimester, which makes it easier to establish the
diagnosis of associated fibroids, with the uterus and pregnancy being small. More-so,
this was due to patient’s anxiety as she was bleeding knowing that she was pregnant
for the first time which made her seek medical intervention.
The main effect of pregnancy on fibroids is related to the size of the uterine fibroids.
For decades, scientists have debated whether hormonal changes that occur during
pregnancy can affect the sizes of uterine fibroids. Uterine fibroids were considered to
enlarge during pregnancy for several decades, especially during the first trimester.
Benaglia et al., in their prospective cohort study on 25 women with fibroids, reported
that, during the first 7 weeks of pregnancy, the sizes of the fibroids grew significantly
to more than double their initial sizes. This therefore calls for the need to book follow-
up scans to assess the progression of pregnancy and monitoring the growth of the
identified fibroids.
Changes in gestational sac shape seen during scanning may be caused by external
compression due to an over-distended bladder or bowel or to fibroids in the uterine
wall. Myometrial contractions may distort the sac shape in the first trimester.
Ultrasound, which is utilised as a first diagnostic tool for myomas, is used to screen
them. The accuracy of diagnosis, size, and position of these fibroids tumours, as well
as differentiation from an adnexal mass, has greatly increased since the debut of MRI
scan as a diagnostic tool. However, MRI has been described as the most expensive
technology used for analysing uterine fibroid.
MANAGEMENT
Because of the high likelihood of uterine problems such as necrosis and malignant
transformation of benign fibroid tumours, treatment of uterine fibroids should be
tailored to the size and location of the tumour, patient’s age, presenting symptoms,
desire to maintain fertility and the gynaecologicals experience. Uterine artery
embolization, ablative treatments, expectant care, surgery, and medicinal management
are all options for treating this fibroid. Conservative, medicinal, or surgical treatment
options are available.
Patients who are asymptomatic are treated conservatively. This includes periodic
explanations, reassurances, and re-examinations. If anaemia is discovered in
symptomatic cases of menorrhagia, it should be treated. Menorrhagia can be treated
with tranexamic acid, combined oral contraceptives, or a levonogestrel-releasing
intrauterine device. Prescription of agonadotropin-releasing hormone analogue, which
has been used to limit oestrogen production and, as a result, reduces the mass of
existing fibroids, making them suitable for laparoscopic surgery.
In order to maintain productiveness and menstrual function in young female patients,

proper counselling and the possibility of myomectomy is recommended in patients
with symptomatic fibroids as well as those with large, asymptomatic fibroids.
Females who want to keep their fertility and uterus should have their treatment
focused on improving symptom alleviation and quality of life.
CONCLUSION
Because of the risk of excessive haemorrhaging, obstetricians usually avoid the
removal of uterine fibroids during cesarean deliveries unless they are tiny and
pedunculated. Despite the fact that the majority of fibroids are asymptomatic, their
location and size may have an impact on the pregnancy and delivery process.
Performing routine myomectomies during cesarean section is not indicated, but it is a
feasible and safe technique in some cases, with a good prognosis for the patient.
Consequently, the decision of performing myomectomies during pregnancy can be a
challenge and must be performed for select cases. This procedure may have several
benefits, such as avoiding another operation to remove fibroids. Therefore ultrasound
plays an important role in obstetrics for the evaluation of fibroids, their location as
well as their number for monitoring their growth and planning of mode of delivery
appropriately.
REFERENCES:
1. Chudleigh T and Thilaganathan B. (2004): Obstetric Ultrasound: How, Why

and When. 3rd edn, Elsevier, Edinburgh London New Yolk Oxford Philadelphia St
Louis Sydney Toronto.
2. Klatsky, P. C.; Tran, N. D.; Caughey, A. B.; Fujimoto, V. Y. (2008): Fibroids
and Reproductive Outcomes: A Systematic Literature Review from Conception to
Delivery. Am. J. Obstet. Gynecol. 2008, 198, 357–366. [Google Scholar] [CrossRef].
3. Kurjak, A and Chervenak, F. A. (2011): Donald School Textbook of
Obstetrics and Gynaecology. 3rd Edn, Jaypee Brothers Medical Publishers (P) Ltd.
New Delhi. Panama Cityu. London.
4. Parker, W. H. (2007): Etiology, Symptomatology, and Diagnosis of Uterine
Myomas. Fertil. Steril. 2007, 87, 725–736. [Google Scholar] [CrossRef] [PubMed]
5. Puscheck, E. E.; Diamond, M. P. (2012): Adverse Obstetric Outcomes
Associated with Sonographically Identified Large Uterine Fibroids. Fertil.
Steril. 2012, 97, 107–110. [Google Scholar] [CrossRef].
6. Sanders, R. C. and Winter T. C. (2007): Clinical sonography: a practical
guide. 4th edn, Lippincott Williams & Wilkins, Philadelphia.
7. Shavell, V. I.; Thakur, M.; Sawant, A.; Kruger, M. L.; Jones, T. B.; Singh, M.;
Pavone, D.; Clemenza, S.; Sorbi, F.; Fambrini, M.; Petraglia, F. (2018):
Epidemiology and Risk Factors of Uterine Fibroids. Best Pract. Res. Clin. Obstet.
Gynaecol. 2018, 46, 3–11. [Google Scholar] [CrossRef] [PubMed]
CASE STUDY-UTERINE FIBROIDS/LEIOMYOMAS
INTRODUCTION
Uterine fibroids, otherwise known as myomatous or leiomyoma, are benign,

monoclonal tumours of the smooth muscle cells of the human uterus (Parker, 2007;
Kempson and Hendrickson, 2000). They are the most common tumours in women of
reproductive age and are asymptomatic in at least 50% of afflicted women (Gupta et
al,. 2008). Symptoms include menstrual disturbances such as menorrhagia,
dysmenorrhea and intermenstrual bleeding (Gupta et al., 2008); dyspareunia and non-
cyclic pelvic pain (Lippman et al., 2003) and pressure symptoms such as a sensation
of bloatedness, increased urinary frequency, and bowel disturbance are also common
(Ciavattini et al., 2013). It may also impair reproductive functions resulting in reduced
fertility, early pregnancy loss, increased preterm labour and delivery, and markedly
increase the risk for cesarean delivery (Payson et al., 2006, Ciavattini et al., 2013).
Fibroids according to (Sanders R.C. and Winter T.C, 2007); are classified based on
their location in relation to the endometrial cavity as:
 Submucosal - fibroids, which border on the endometrial cavity, often cause
frequent lengthy periods with intramenstrual spotting and may cause in fertility.
 Intracavitary- Fibroids that lie within the cavity or protrude into the cavity which
are even more likely to cause vaginal bleeding and cramping.
 Pedunculated- Fibroids that have a small neck and extend to the border of the
uterus. They may be hard to distinguish from adnexal masses and may twist and
infarct (torsion).
Several factors have been implicated in the etiology of fibroids. Epidemiological

studies have linked fibroids to the female reproductive hormones, oestrogens, and
progesterone. Oestrogens and their receptors are reported to exert a great influence on
fibroid growth. Several studies found that memory ribonucleic acid (mRNA) and
protein expression levels as well as the content of oestrogen receptor-alpha (ER-a)
and ER-[sz] are higher in leiomyoma compared to those in normal myometrium
(Benassayag et al., 1999; Kovacs et al., 2001). Oestrogens, it is hypothesized, may
exert their growth stimulatory effects on leiomyomas intermediated by cytokines,
growth factors, or apoptosis factors (Grings et al., 2012).
The role of progesterone in the etiology of fibroids is through its interaction with its
receptors, progesterone receptor-A (PR-A) and PR-B (Kastner et al., 1990).
Leiomyomas are known to have higher PR content and mRNA levels compared to
normal myometrium (Viville et al., 1997; Ying and Weiyuan, 2009). This is further
buttressed by the relative over-expression of PR-B mRNA in the surface of
leiomyoma as described by Fujimota et al., (1998).
A 49 year old patient in this case presented the Gynaecology OPD with a painful mass
in lower abdomen with gradual enlargement of abdomen for last 7 months. She had a
clinical history of nausea, vomiting, weight loss, loss of appetite, pain in the lower
abdomen, intermenstrual bleeding and intermittent constipation.
INDICATION
 Abnormal uterine bleeding ???. Rule out uterine fibroids/pelvic pathology.
Examination Date: 26 July 2022
PATIENT INFORMATION
Date of Birth 27 August 1973
Parity 3
Gravida 5
Last Menstrual Period Unknown
Contraceptive Nil
Marital Status Married
Sex Female
Level of Education Ordinary Level
EQUIPMENT
 Mindray DC-6 Ultrasound machine.
 3.5-5MHz curvilinear probe .
 Sony High glossy thermal paper.
 Ultrasound gel.
 Sony Ultrasound Printer.
Standard gynaecological transabdominal scan protocol documented in appendix B
attached
There was a bulky anteverted and non-gravid uterus with a heterogeneous echotexture
measuring 11.14 cm x 6.42 cm x 9.93 cm. The uterus had an irregular shape with well
defined margins and a short normal cervix.
 A symmetrical, well-defined, heterogeneous, solitary solid mass measuring 7.76
cm x 6.55 cm x 7.99 cm was seen occupying the myometrial layer of the uterus.
The intramural heterogeneous mass appeared as if it enclosed two echogenic
distinct masses with hypoechoic margins pushing the urinary bladder anteriorly.
 The intramural mass does not cover the cervix though it occupies the anterior and
posterior aspects of the myometrium.
 The endometrium was not visualised
 Color Doppler ultrasound showed the fibroid’s circumferential vascularity.
 Pulsed wave Doppler was not used to assess the waveform of the feeding vessels.
 The ovaries were not visualised and there were no adnexal solid or cystic masses
seen.
 The urinary bladder was distended with a relatively smooth mucosal outline and
its contents were not visualised hence its integrity was not assessed.
 There was no free fluid in the pouch of Douglas.
 There was a complex cystic abdominal mass seen antero-lateral to the uterus
with an echogenic irregular central intact solid mass. It measured 9,89 cm x 4,38
cm. Its length extends from the midline to the midclavicular line on the right
lower quadrant.
 There was evidence of peripheral vascularity on color Doppler interrogation.
Uterine Measurements
Serial Parameter Measurement (cm)
(a) (b) (c)
1. Uterine length 11.4
2. Uterine width 9.93
3. Uterine height 6.42
4. Uterine volume 371.2 cc
5. Uterine body 27.49
Comment
1. Bulky non gravid fibroid uterus.
2. An intramural symmetrical, well-defined, heterogeneous, solitary solid mass
measuring 7.76 cm x 6.55 cm x 7.99 cm occupies the entire myometrium.
3. Complex cystic pelvi-abdominal mass measuring 9,89 cm x 4,38 cm.
4. Ultrasound guided biopsy is recommended.
5. Differential diagnosis could be:
 Uterine lipoleiomyoma.
 Focal adenomyosis.
 Uterine leiomyosarcoma; though rare.
Correlate clinically.
DISCUSSION
Etiology and Pathophysiology

Although, the exact etiology of fibroid is not known yet, the growth of uterine fibroid
is featured as a benign, hormone sensitive diffuse or nodulus hyperplasia of
myometrium, and is characterized by having multiple factors of pathogenesis and
systemic changes. Uterine fibroid is developed on the background of hyperestrogens,
progesterone deficits and hypergonadotropins.
The role of ovarian steroid hormones in the pathogenesis of uterine fibroids is

supported by epidemiological, clinical, and experimental evidence. Estradiol
and progesterone induce mature leiomyoma cells to release mitogenic stimuli to
adjacent immature cells, thereby providing uterine leiomyoma with undifferentiated
cells that are likely to support tumour growth.
Progesterone action is required for the complete development and proliferation of
leiomyoma cells, while estradiol predominantly increases tissue sensitivity to
progesterone by increasing the availability of progesterone receptors (PRs).
The selective estrogen receptor modulator (SERM) raloxifene and the selective PR
modulators (SPRMs) mifepristone, asoprisnil, and ulipristal acetate have been shown
in clinical trials to inhibit fibroid growth. The role of sex steroids is critical for
leiomyoma development and maintenance, but a number of autocrine and paracrine
messengers are involved in this process; hence, numerous pathways remain to be
explored in therapeutic innovations for treating this common disease. The majority of
the researchers consider that the growth of fibroid depends on concentration of
cytosolic receptors to the sexual hormones and their interactions with the endogenous
or exogenous hormones. In accordance to clinical observations, it can be admitted that
both growth and regression of fibroid are oestrogen-dependant; the tumour size gets
increased during pregnancy and is regressed after menopause.
em
Risk factors
Even if many risk factors suggested by epidemiology studies have linked uterine
leiomyomas to the effects of oestrogen and progesterone levels and their metabolism,
other mechanisms may be involved in fibroids pathogenesis. In fact, recently,
Peddada et al. have questioned the exact role of female hormones (oestrogens and
progesterone) in the development and growth of uterine fibroids. The authors
measured the growth of fibroids in black and white women with clinically relevant
fibroids using MRI technology; they demonstrated that fibroids within the same
woman often have different growth rates despite having a similar hormonal milieu. In
the same patients, fibroids were found to vary in size, regress, or remain stable. Each
tumour appeared to have its own intrinsic growth rate, and fibroid growth appeared
not to be influenced by tumour characteristics such as size and location.
It has been generally accepted that myomas are more prevalent in blacks than in
Caucasian and Hispanic populations (Kjerulff, K. H. et al 1996). Although the cause
of the higher prevalence among black women is unclear, differences in circulating
oestrogen levels have been found. It is still unclear (Parker, W. H. 2007) whether
these ethnical differences are genetic or due to known variations in hormonal
metabolism, diet, or environmental factors.
Leppert et al. reported that the pathogenesis of fibroids seems to involve a positive
feedback loop between extracellular matrix production and cell proliferation, and
vitamin D might act to block the positive feedback. It is also interesting that myomas
and keloids, both more common in black women, have similar gene characteristics.
Furthermore, it is well known that family history could represent a strong
predisposing factor; the first-degree relatives of affected women have a 2.5 times
increased risk of developing fibroids. However, as recently reported from Saldana et
al., such bias would invalidate self-reported family history as a predictor of fibroid
risk (Saldana. T.M. 2013).
Patient Presentation
Abnormal uterine bleeding and intermenstrual bleeds are common symptoms of
uterine fibroids. Other symptoms however, include anaemia, back pain, pelvic pain
and pressure, constipation, urinary frequency/retention, miscarriages, or infertility.
These characteristic symptoms resembles those of 49 years old patient in this case
who presented to the Gynaecology OPD with a painful mass in lower abdomen with
gradual enlargement of abdomen for last 7 months. She had a clinical history of
nausea, vomiting, weight loss, loss of appetite, pain in the lower abdomen,
intermenstrual bleeding and intermittent constipation.
ULTRASOUND FEATURES OF UTERINE FIBROIDS

Sanders R.C. and Winter T.C, 2007 describe the sonographic features of uterine
fibroids as:
 An enlarged uterus, usually with a lobulated contour that may indent the urinary
bladder. If the urinary bladder volume is small, documentation of the size
becomes paramount. Thus frequency is a common complication of fibroids
because they reduce urinary bladder capacity.
 Focal ovoid or circular masses within the uterus. These masses may have a
similar echogenicity to the remainder o the uterus, but tissue within is organized
in a whirled (circular) fashion. Blood vessels form a rim around the fibroid,
whereas with other entities, they may look similar, such as in focal adenomyosis
in which blood vessels traverse the lesion.
 The fibroid may be surrounded with a rim of calcification that can occasionally
be so dense that the centre cannot be seen with ultrasound.
Other sonographic features relate to the classification of fibroids in relation to
endometrial cavity as already elucidated in the paragraphs above. It then suffice to
note that ultrasound was very useful in the diagnosis of fibroids in this patient as she
had typical symptoms and sonographic appearances of fibroids as those found in
literature.
MANAGEMENT
Because of the high likelihood of uterine problems such as necrosis and malignant
transformation of benign fibroid tumours, treatment of uterine fibroids should be
tailored to the size and location of the tumour, patient’s age, presenting symptoms,
desire to maintain fertility and the gynaecologicals experience. Uterine artery
embolization, ablative treatments, expectant care, surgery, and medicinal management
are all options for treating this fibroid. Conservative, medicinal, or surgical treatment
options are available.
Patients who are asymptomatic are treated conservatively. This includes periodic
explanations, reassurances, and re-examinations. If anaemia is discovered in
symptomatic cases of menorrhagia, it should be treated. Menorrhagia can be treated
with tranexamic acid, combined oral contraceptives, or a levonogestrel-releasing
intrauterine device. Prescription of agonadotropin-releasing hormone analogue, which
has been used to limit oestrogen production and, as a result, reduces the mass of
existing fibroids, making them suitable for laparoscopic surgery.
In order to maintain productiveness and menstrual function in young female patients,

proper counselling and the possibility of myomectomy is recommended in patients
with symptomatic fibroids as well as those with large, asymptomatic fibroids.
Females who want to keep their fertility and uterus should have their treatment
focused on improving symptom alleviation and quality of life.
CONCLUSION
Because of the risk of excessive haemorrhaging, obstetricians usually avoid the
removal of uterine fibroids during cesarean deliveries unless they are tiny and
pedunculated. Despite the fact that the majority of fibroids are asymptomatic, their
location and size may have an impact on the pregnancy and delivery process.
Performing routine myomectomies during cesarean section is not indicated, but it is a
feasible and safe technique in some cases, with a good prognosis for the patient.
Consequently, the decision of performing myomectomies during pregnancy can be a
challenge and must be performed for selected cases. This procedure may have several
benefits, such as avoiding another operation to remove fibroids. Therefore ultrasound
plays an important role in obstetrics and gynaecology for the diagnosis and evaluation
of fibroids, their location as well as their number for monitoring their growth and
planning of mode of management appropriately.
REFERENCES:
1. Chudleigh T and Thilaganathan B, 2004. Obstetric Ultrasound: How, Why and

When. 3rd edn, Elsevier, Edinburgh London New Yolk Oxford Philadelphia St Louis
Sydney Toronto.
2. Gupta, S,; Jose, J,; Manyonda, I. (2008): Clinical presentation of fibroids. Best
Practice & Research Clinical: Obstetrics & Gynaecology. 2008;22(4):615-26.
3. Klatsky, P.C.; Tran, N.D.; Caughey, A.B.; Fujimoto, V.Y.(2008): Fibroids
and Reproductive Outcomes: A Systematic Literature Review from Conception to
Delivery. Am. J. Obstet. Gynecol. 2008, 198, 357–366. [Google Scholar] [CrossRef].
4. Kurjak, A and Chervenak, F. A. (2011); Donald School Textbook of
Obstetrics and Gynaecology. 3rd Edn, Jaypee Brothers Medical Publishers (P) Ltd.
New Delhi. Panama City. London.
5. Parker, W.H. (2007): Etiology, Symptomatology, and Diagnosis of Uterine
Myomas. Fertil. Steril. 2007, 87, 725–736. [Google Scholar] [CrossRef] [PubMed]
6. Puscheck, E.E.; Diamond, M.P.(2012): Adverse Obstetric Outcomes
Associated with Sonographically Identified Large Uterine Fibroids. Fertil.
Steril. 2012, 97, 107–110.
[Google Scholar] [CrossRef].
7. Sanders R.C. and Winter T.C. (2007): Clinical sonography: a practical guide.
4th edn, Lippincott Williams & Wilkins, Philadelphia.
8. Shavell, V.I.; Thakur, M.; Sawant, A.; Kruger, M.L.; Jones, T.B.; Singh, M.;
Pavone, D.; Clemenza, S.; Sorbi, F.; Fambrini, M.; Petraglia, F.(2018): Epidemiology
and Risk Factors of Uterine Fibroids. Best Pract. Res. Clin. Obstet.
Gynaecol. 2018, 46, 3–11. [Google Scholar] [CrossRef] [PubMed]
CASE STUDY-MOLAR PREGNACY
INTRODUCTION
First-trimester pregnancy is defined as the first 12 weeks after the patient’s last
menstrual period. It is the period of human development associated with the highest
complication rate. During this critical period, ultrasound may be used to confirm
intrauterine pregnancy, determine viability, and exclude ectopic pregnancy or
gestational trophoblastic disease (GTD).
A molar pregnancy also known as hydatidiform mole is a rare complication of

pregnancy characterized by the abnormal growth of trophoblasts, the cells that
normally develop into the placenta. Molar pregnancy (molahydatidosa) belongs to a
group of diseases classified as gestational trophoblastic disease resulting from
abnormal fertilization (Dr. Gupta, A. et al. 2019). It is divided into two types -
complete and partial molar pregnancy, based on distinctive histopathological features
and genetic abnormalities. GTD includes a spectrum of tumours that can be benign or
malignant. Benign entities include complete and partial moles.
A complete mole may be seen as an intrauterine mass with cystic spaces without any
associated foetal parts. In comparison, a partial mole may be visualized as a
gestational sac containing amorphous echoes representing foetal parts with an
enlarged cystic placenta. Pathogenetically, it is a complete or partial trophoblastic
proliferation (of cyto- and syncytiotrophoblasts) with hydropic degeneration of the
placental villi.
Complete molar pregnancy usually occurs when an egg without maternal

chromosomes is fertilized by a single sperm, with a subsequent duplication of its
DNA, resulting in a 46, XX paternal karyotype. Abnormal fertility is associated with a
maternal autonomic recessive mutation, most commonly NLRP7 on chromosome
19q, leading to recurrent molar pregnancies. As a result, hydropic trophoblastic
degeneration and lack of embryonic structures develop (Hancock, B. W. and Tidy, J.
A. 2002).
According to Malhotra, N. et al. (2002); partial mole is a result of fertilization of a
haploid normal oocyte with two spermatozoa simultaneously, with the formation of a
zygote with a triploid set of chromosomes (69 XXX, 69XXY or 69 XYY) and is most
often associated with the development of an irregularly shaped foetus. A possible
variant is also a partial hydropic degeneration of the placenta resulting in a foetus with
a diploid chromosome set. Not infrequently, partial molar pregnancy remains
undiagnosed in cases with first trimester pregnancy loss in the form of incomplete or
missed abortion. Medical literature report that in less than 25% of cases, partial mole
occurs with the development of an euploid viable foetus, with the following options
possible: most often it is a twin pregnancy, with one gestational sac containing normal
foetus with normal placenta and the other one with a complete molar pregnancy; the
second type is a twin pregnancy with one of the foetuses being normal with a normal
placenta and the other sac having an incomplete mole.
A molar pregnancy can have serious complications including a rare form of cancer
and requires early treatment. The majority of complete moles present with vaginal
bleeding and markedly elevated beta-human chorionic gonadotropin (b-hCG) values.
A molar pregnancy may seem like a normal pregnancy at first, but most molar
pregnancies cause specific signs and symptoms, including: dark brown to bright red
vaginal bleeding during the first trimester, severe nausea and vomiting, sometimes
vaginal passage of grape-like cysts, pelvic pressure or pain. Other signs are rapid
uterine growth where the uterus is too large for the stage of pregnancy, high blood
pressure, pre-eclampsia- a condition that causes high blood pressure and protein in the
urine after 20 weeks of pregnancy, ovarian cysts, anaemia and over-active thyroid
(hyperthyroidism).
Case Presentation: A 28 years old black African lady of unknown LMP, Para 2
Gravida 3 with positive pregnancy test done a week prior to her visit presented to the
Radiology Department complaining of vaginal bleeding and history of treated vaginal
discharge, nausea, vomiting and abdominal fullness. On physical examination, she
was anaemic, with raised BP, and relatively unstable. The physical pelvic exam had
revealed a small amount of dark blood without signs of active bleeding, an anteverted
uterus of eight weeks size and a closed cervix. She had no laboratory results of
quantitative beta-human chorionic gonadotropin levels and was referred by a General
Practitioner for ultrasound of the pelvis to rule out miscarriage.
INDICATION
 First trimester obstetric scan to rule out early pregnancy miscarriage.
Date Of Examination: 15 August 2022
PATIENT INFORMATION
Date of Birth: 16 December 1994

Parity: 2
Gravida: 3
LMP: Unknown
Contraception: Nil
Marital status: Single
Sex: Female
Level of Education: Ordinary Level
EQUIPMENT
Mindray DC-6 Ultrasound machine.
3.5-5MHz curvilinear probe .
Sony High glossy thermal paper.
Ultrasound gel.
Sony Ultrasound Printer.

Standard First Trimester Obstetric Transabdominal Scan Protocol documented in
appendix B attached.
 The uterus was bulky, anteverted, non- gravid(with no visible GS) and non
fibroid and bulky measuring 9.34 cm x 7.55 cm x 8.20 cm with a heterogeneous
echotexture.
 A predominantly solid, large central heterogeneous echogenic mass that expands
the endometrial canal with multiple solid cystic spaces and no identifiable foetal
parts or gestational sac was seen occupying the entire bulky uterus.
 The intrauterine mass contained multiple cystic spaces of varying sizes from 0.6
to 0.8 cm and it demonstrated a snowstorm appearance with both peripheral and
intra-mass vascularity on color Doppler.
 Pulsed wave Doppler of a peripheral artery demonstrated high velocity of 28.61
cm/s.
 A left ovarian unilocular hypoechoic complex cystic mass measuring 3.13 cm in
the short axis and 1.75cm in long axis was seen. The cystic ovarian mass
demonstrated posterior enhancement and peripheral vascularity on color Doppler
interrogation. The right ovary appeared normal in size and echogenicity.
 The urinary bladder was partial distended hence it was not assessed.
 No evidence of pelvic free fluid, or any free fluid collections seen in the POD.
 No evidence of ectopic pregnancy seen sonographically.
COMMENT
 A predominantly solid, large central heterogeneous echogenic intrauterine mass
that expands the endometrial canal with innumerable uniformly distributed cystic
spaces and no identifiable foetal parts or gestational sac is highly suggestive of
complete molar pregnancy/ hydatidiform mole.
 A left ovarian unilocular hypoechoic complex cystic mass measuring 3.13 cm in
the short axis and 1.75cm in long axis is highly suggestive of left ovarian theca
luteal cyst.
 No evidence of PID / ectopic pregnancy shown by ultrasound.
 Recommend laboratory tests of quantitative beta-human chorionic
gonadotropin levels and a CT scan /PET scan to stage the disease.
 Rescan after seven days with laboratory results of quantitative beta-human
chorionic gonadotropin levels.
 Differential Diagnosis is of Abnormal villous morphology; or Early abortus with
trophoblastic hyperplasia; or Hydropic abortus.
 Clinical correlation highly advised.
DISCUSSION
Pathophysiology
A molar pregnancy is a rare complication of pregnancy characterized by the abnormal
growth of trophoblasts, the cells that normally develop into the placenta. In Europe,
North and South America, (Kubelka-Sabit, K.B., et al., (2017); reported that
hydatidiform moles observed in approximately 1 in every 1,000 pregnancies are
diagnosed as a molar pregnancy and the prevalence is 5 to 15 fold higher in East Asia.
In a complete molar pregnancy, an empty egg is fertilized by one or two sperm, and
all of the genetic material is from the father. In this situation, the chromosomes from
the mother's ovum are lost or inactivated and the father's chromosomes are duplicated,
thus, only paternal DNA is expressed. This most often occurs when two sperms
fertilise an egg/ovum, resulting in an extra copy of the father's genetic material
(Lurain, J. R. 2010). The karyotype of complete moles is usually 46,XX 90% of the
time and 46,XY 10% of the time; the chromosomes derived completely from the
father as a complete mole likely results from the fertilization of anuclear empty ovum
by a haploid sperm that duplicates its own chromosomes after meiosis.
On the other hand, in partial moles, the karyotype is 90% of the time triploid and
either 69,XXX or 69,XXY. This karyotype arises when a normal sperm subsequently
fertilizes a haploid ovum duplicates and or when two sperms fertilize a haploid ovum.
In partial moles, both maternal and paternal DNA is expressed.
Histopathology
 Hydatidiform mole is characterized by an overgrown villous trophoblast with
cystic "swollen" villi which macroscopically can be visible in the
second trimester, as clusters of vesicles (similar to small grapes) developed from
the transformation of chorionic villi. Complete mole differs from partial mole, in
cytogenetic and microscopical appearance. Important is a complete lack of
embryonic/foetal tissue in complete moles and the presence of embryonic tissue
in partial moles.
 Microscopically, a complete mole has markedly hydropic and deformed chorionic
villi with the formation of "cisterns" containing stromal fluid; there is a
peripheral proliferation of both cytotrophoblast and syncytiotrophoblast, arranged
in lace-like structures, papillary formation, or circumferential. In normal early
placenta the cytotrophoblast and syncytiotrophoblast are polarized. There is the
absence of foetal stromal blood vessels. An immature vascular network is
otherwise present, positive for CD31, with dysmorphic features such as a
complete lack of lumen.
 In partial mole, there are hydropic chorionic villi surrounded by hyperplastic
trophoblasts with variable degrees of central cistern formation, with an irregular
maze-like pattern; also, there are normal chorionic villi and embryonic or foetal
tissue mixed with hydropic villi. There are recognizable foetal blood
vessels containing foetal red blood cells. The curettage material should be
examined carefully, especially in first trimester pregnancies, and if a partial mole
is suspected the whole specimen should be examined.
 The main differential diagnosis is with a hydropic abortion, where the main clue
is the presence of villous oedema only with microscopical evaluation and lacks
cistern formation or trophoblastic proliferation.
 A pitfall in hydropic abortion is the presence of polar stratification of anchoring
trophoblast in a first-trimester placenta. The villous size in hydropic abortion
ranges from small, to medium and large.
 An important marker that aids in the diagnosis of the complete mole is the
presence or absence of p57 in immunohistochemistry. This marker is a paternal-
imprint inhibitor gene so its expression implies the maternal contribution; in
brief, the absence of p57 expression supports the diagnosis of androgenetic
gestational disease with complete mole (Xing, D. et al. 2021). Moles also
express p53, p21, cyclin E, and MCM7.
ULTRASOUND FEATURES OF MOLAR PREGNANCY

 In a complete mole, the ultrasound findings include a heterogeneous mass in the
uterine cavity with multiple anechoic spaces, most commonly referred to as a
"snowstorm" appearance. These small cystic areas are typically the hydropic villi
described previously in the histopathology section. Furthermore, there is the
absence of an embryo or foetus, and no amniotic fluid is present.
 In a partial mole, there typically is the finding of a foetus which may be viable,
the presence of amniotic fluid, and the placenta appears to have enlarged, cystic
spaces (often described as "Swiss cheese" appearance). In one study, it was noted
that partial moles were diagnosed as a missed or incomplete abortion in 15% to
60% of cases.
NB: If a molar pregnancy is diagnosed, the next step is typically a CT scan and PET
scan to stage the disease. Furthermore, a chest x-ray should be obtained if the
patient's initial symptoms included any signs of respiratory distress or increased
breathing to evaluate for pulmonary oedema.
Patient Presentation
The case presentation of a 28 year old pregnant black African woman with complete
molar pregnancy after ultrasound scan, a history of unknown LMP, Para 2 Gravida 3
with positive pregnancy test done a week prior to her visit; complaining of vaginal
bleeding and history of treated vaginal discharge, nausea, vomiting and abdominal
fullness. On physical examination, she was anaemic, with raised BP, and relatively
unstable. The physical pelvic exam had revealed a small amount of dark blood
without signs of active bleeding, an anteverted uterus of eight weeks size and a closed
cervix. She had no laboratory results of quantitative beta-human chorionic
gonadotropin levels.
Transabdominal ultrasound revealed an anteverted, non- gravid(with no visible GS)

and non fibroid and bulky measuring 9.34 cm x 7.55 cm x 8.20 cm with a
heterogeneous echotexture. A predominantly solid, large central heterogeneous
echogenic mass that expands the endometrial canal with multiple solid cystic spaces
and no identifiable foetal parts or gestational sac was seen occupying the entire bulky
uterus. The mass contained multiple cystic spaces of varying sizes from 0.6 to 0.8 cm.
The mass demonstrated a snowstorm appearance with both peripheral and intra-mass
vascularity on color Doppler. Pulsed wave Doppler of a peripheral artery
demonstrated high velocity of 28.61 cm/s. A left ovarian unilocular hypoechoic
complex cystic mass measuring 3.13 cm in the short axis and 1.75cm in long axis was
seen. The theca leuteal cyst demonstrated posterior enhancement and peripheral
vascularity on color Doppler interrogation.
Case Discussion:
 A significant risk factor for the development of complete molar pregnancy is the
age of the mother. Compared with the risk in women aged 21 to 35 years, the risk
is 1.9 times higher for women 35 years, and 7.5 times higher for women>40
years, including 1 in 3 pregnancies for women>50 years (MOJ Anat Physiol.
2020;7(5):150‒153).
 The transabdominal ultrasound findings obtained are consistent with what is
documented in medical and reviewed literature above. However, such a
dependence is not established with regard to the risk of developing a partial mole.
Partial molar pregnancy is more common in women with a history of irregular
menstruation, miscarriage and oral contraceptives for more than 4 years, while
ethnicity, dietary factors and ovulation induction are not associated with an
increased risk.
 Complete molar pregnancy is most often presented by vaginal bleeding at 6 - 16
weeks of gestation in 90% of cases. Other classic symptoms, such as higher than
expected gestational age, hyperemesis, hyperthyroidism and trophoblastic
embolization are less common in the first trimester and in recent years due to
earlier diagnosis, as a result of the widespread use of high-quality/resolution
ultrasonography and quantitative measurement of human chorionic gonadotropin
(hCG). Complete molar pregnancy is also associated with a similar clinical
manifestation.
 In addition to the typical clinical manifestation as a result of excessive hCG
production, molar pregnancy is characterized by a specific ultrasound features.
These typical ultrasound manifestations of a complete molar pregnancy include
the visualization of a diffuse, multi-cystic and often hyper-vascular intrauterine
mass (“snowstorm” or “honeycomb” type) with no foetal tissues. Partial molar
pregnancy may present as a localized placental abnormality with a living embryo,
spontaneous intrauterine foetal death, or the presence of an empty gestational sac
(blighted ovum).
 Some authors propose the following ultrasound criteria for specific findings of
partial molar pregnancy as a ratio of transverse to Antero-posterior diameter of
the gestational sac >1.5 and cystic changes in the placenta and/or irregularity of
the contour of the decidua, placenta or myometrium (Kirk, E. 2007).
 During the first trimester, the frequency of diagnosing a complete mole is higher
than that of a partial mole, increasing with advancing of gestational age. Fowler
D. J., et al. (2006); analysed 378 ultrasound-proven molar pregnancies,
demonstrating the accuracy of the ultrasound diagnosis in 200 of 253 (79%)
complete hydatidiform moles and 178 of 616 (29%) partial hydatidiform
pregnancies.
 Several factors determine the prognosis of a foetus in a partial molar pregnancy,
such as the karyotype of the foetus, the size of the area with hydropic
degeneration of the placenta, the rate of hydropic degeneration and the
manifestation of foetal anaemia or other obstetric complications such as pre-
eclampsia, thyrotoxicosis and vaginal bleeding.
 According to Hsieh, C. C., et al. (1999); in singleton pregnancies with dizygotic
normal foetus with partial molar placenta, pregnancy development depends on the
genesis of placental degeneration, from amniotic diploidy to chorionic villus
triploidy, which determines two different types of placental pathology: focal and
diffuse partial degeneration. In most cases, however, the diagnosis of a partial
mole is in the case of intrauterine foetal death.
 Despite early diagnosis of complete mole, which leads to fewer complications, no
concomitant reduction in the incidence of post-molar gestational trophoblastic
neoplasia (GTN) has been observed [Fowler D. J., et al. (2006)]; approximates
that 10% to 20% of women with a complete molar pregnancy and 0.5% to 11%
with a partial molar pregnancy will continue to develop persistent, invasive
gestational trophoblastic disease, including invasive mole, choriocarcinoma, or
placental trophoblastic tumour.
 In case of a suspected diagnosis of molar pregnancy on the basis of medical
history, physical examination, hCG level and ultrasound findings, the physician
should assess the presence of medical complications (anaemia, pre-eclampsia,
hyperthyroidism) which have to be treated.
 Key diagnostic and laboratory tests include: complete blood count, complete
metabolic panel, thyroid function test, urine test, chest x-ray, an
electrocardiogram, coagulation status and blood group with rhesus factor.
The case under discussion therefore was positive for the ultrasound and clinical
presentation of complete molar pregnancy diagnosed in the first trimester.
MANAGEMENT
Patients who are diagnosed with molar pregnancy must be evaluated for possible
complications such as: Over-active thyroid, anaemia, and toxaemia of pregnancy.
Patients should have a complete examination and laboratory testing [Lurain, J. R.
(2010)]. After any medical complications have been addressed, a decision must be
made concerning the best method of evacuation.
Suction curettage is the optimal method of evacuation, regardless of uterine size, in

patients who wish to retain reproductive function, because it carries a significantly
lower risk of excessive bleeding, infection, and retained molar tissue than methods
involving induction with oxytocin or prostaglandin. Rh immune globulin should be
given to patient with RH conflict.
Maximum dilatation of the cervical canal and aspiration with a 12- to 14-millimeter
cannula under ultrasound control are recommended. As the risk of excessive bleeding
increases with the size of the uterus, it is necessary to provide at least two sacks of
blood preoperative in cases with uterine size >16 gestational weeks.
Hysterectomy is an alternative in patients who do not wish to maintain fertility or who

are at increased risk of developing post-molar gestational trophoblastic disease.
Adnexa can be preserved bilaterally, even in the presence of theca-lutein cysts. In
addition to the evacuation of molar pregnancy, hysterectomy provides permanent
sterilization and eliminates the risk of local myometrial invasion as a cause of
persistent mole. Due to the possibility of metastasis even after hysterectomy, the risk
of post-molar gestational trophoblastic disease still remains between 3% and 5%, thus
requiring long term follow-up of hCG [Lurain, J. R., (2011)].
Drug induction and hysterectomy as proposed by Ngan, H. Y. S., et al. (2003); are
not recommended for termination of molar pregnancy. These methods increase
maternal morbidity, such as excessive blood loss, incomplete evacuation requiring
curettage and the need for cesarean delivery in subsequent pregnancies. Prophylactic
chemotherapy during or immediately after evacuation of molar pregnancy is
associated with a reduction in the incidence of persistent mole from approximately
20% to 3%. Chemotherapy is recommended in high-risk patients (age>40 years,
hCG>100,000 mIU/mL, uterine enlargement, theca luteal cysts >6 cm, medical
complications) and/or when adequate hCG monitoring is not possible.
After termination of molar pregnancy, follow-up is essential for the detection of
trophoblastic disease (invasive mole or choriocarcinoma), which develops in
approximately 15% to 20% of patients with a complete mole and 1% to 5% in a
partial mole. Clinically uterine involution, regression of theca-lutein cysts and
cessation of vaginal bleeding are good prognostic signs.
In addition, final follow-up requires serial measurements of serum hCG every 1 to 2

weeks, until three consecutive tests establish normal hCG levels. hCG monitoring
should be determined at 3-month intervals for 6 months after documented negative
values. Contraception is recommended during the follow-up period of 6 months after
the first normal hCG result. Oral contraceptives are preferred because they have the
advantage of suppressing endogenous luteinizing hormone (LH), which may interfere
with the measurement of hCG at low levels.
Indications for treatment of post-molar disease are: plateau of hCG levels within
testing every week for 3 weeks, increase in hCG levels ≥10% with weekly
measurement for 2 weeks, persistently elevated hCG levels 6 months after evacuation,
histopathological diagnosis of choriocarcinoma or trophoblastic tumour or evidence
of metastasis. In all subsequent pregnancies, pathological examination of the placenta
or other products of conception is recommended, as well as monitoring of the hCG
level 6 weeks after birth.
NB: Patients are monitored to prevent the recurrence of benign moles and the
development of malignant neoplasia, which can metastasise to the brain, liver or
lungs. Chest x-rays and the analysis of HCG levels for six months to one year are
necessary]. Recurring moles are treated with methotrexate, a low-level chemotherapy
[Sebire, N. J., and Seckl, M. J. (2008)].
The American College of Obstetricians and Gynaecologists has recommended that

after evacuation of a mole, serum HCG levels should be monitored every 1-2 weeks
in all patients while the levels are elevated and then at monthly intervals for an
additional 6 months once the levels become undetectable (5MIU per millilitre).
 The in this case study was not followed up for management however, she was
recommended for further diagnostic and laboratory tests.
CONCLUSION
While histological diagnosis remains the gold standard for diagnosis, positive
ultrasound features should raise the index of suspicion in cases where the diagnosis is
doubtful. While histological diagnosis remains the gold standard for diagnosis,
positive ultrasound features should raise the index of suspicion in cases where the
diagnosis is doubtful.
In the first few months of pregnancy, molar pregnancy is associated with a higher
incidence of vaginal bleeding or discharge, abdominal pain and morning sickness.
However, as these symptoms are relatively non-specific, they rarely lead to the
diagnosis being made prior to the routine first ultrasound scan.
In complete molar pregnancy, the ultrasound characteristically shows an absent
gestational sac and a complex echogenic intrauterine mass with cystic spaces.
Complete molar pregnancy is associated with marked cystic changes and mass
formation and is often diagnosed ultrasonographically. However, correct prospective
diagnosis was made more frequently in this study than in older reports, perhaps due to
improved spatial resolution of ultrasonographic equipment.
REFERENCE
1. Fowler, D. J., Lindsay, I. and Seckl, M. J. (2006). Routine pre-evacuation

ultrasound diagnosis of hydatidiform mole: experience of more than 1000 cases from
a regional referral center. Ultrasound Obstet Gynecol. 2006;27(1):56–60.
2. Hancock, B. W. and Tidy, J. A. (2002). Current management of molar
pregnancy. J Reprod Med. 2002;47(5):347–354.
3. Hsieh, C. C., Hsieh, T. T. and Hsueh, C. (1999). Delivery of a severely
anaemic foetus after partial molar pregnancy; clinical and ultrasonographic finding.
Hum Repord. 1999;14(4):1122–1126.
4. Kirk, E., Papageorghiou, A. T. and Condous, G. (2007). The accuracy of first
trimester ultrasound in the diagnosis of hydatidiform mole. Ultrasound Obstet
Gynecol. 2007;29(1):70–75.
5. Kubelka-Sabit, K. B. (2017). Molecular and Immunohistochemical
Characteristics of Complete Hydatidiform Moles. Balkan journal of medical genetics :
BJMG, 2017. 20(1): p. 27-34.
6. Lurain, J. R. (2010). Gestational Trophoblastic Disease I: Epidemiology,
Pathology, Clinical Presentation And Diagnosis Of Gestational Trophoblastic
Disease, And Management Of Hydatidiform Mole. Am J Obstet Gynecol 203: 531-
539. [Crossref]
7. Lurain, J. R., (2011). Gestational Trophoblastic Disease. Ii: Classification And
Management Of Gestational Trophoblastic Neoplasia. Am J Obstet Gynecol.
2011;204(1):11–18.
8. Malhotra, N., Deka, D. and Takkar, D. ()2001). Hydatidiform Mole With
Coexisting Live Foetus In Dichorionic Twin Gestation. Eur J Obstet Gynecol Reprod
Biol. 2001;94(2):301–303.
9. Ngan, H. Y. S., Bender, H., and Benedet, J. L., (2003). Gestational
Trophoblastic Neoplasia, Figo 2000 Staging And Classification. Int J Gynecol Obstet.
2003;83:175–177.
10. Sebire, N. J., & Seckl, M. J. (2008). Gestational Trophoblastic Disease:
Current Management Of Hydatidiform Mole. British Medical Journal, 337 (aug15 1),
453-458. doi:10.1136/bmj.a1193
11. NCCN Guidelines: gestational trophoblastic neoplasia. version 1. 2019, 2018.
CASE STUDY- ENDOMETRIAL PYOMETRA
INTRODUCTION
Pyometra is an accumulation of large quantities of purulent exudate in the uterus
causing its distention (Hughes et al. 1979). It must be distinguished from the smaller,
intermittent accumulations of fluid that can be detected by ultrasonography in
acute endometritis. It occurs because of interference with natural drainage of fluid
from the uterus, which may be due to cervical adhesions or an abnormally constricted,
tortuous, or irregular cervix. In some cases, the fluid accumulates in the absence of
cervical lesions, presumably due to an impaired ability to eliminate the exudate; due
to some genital tract malignancy, mainly squamous cell carcinoma of the
endometrium, impairment in the natural drainage through cervix due to stenosis or
neoplasms and the consequences of radiotherapy. Other causes are foreign bodies,
puerperal infections or uterine anomalies.
Pyometra is an uncommon result of endometritis. The diagnosis of pyometra is made

when a collection of pus is found within the endometrial cavity. It has been reported
that pyometra has an incidence of less than 1% of gynaecologic patients. The
incidence of pyometra increases with age and is 13.6% in elderly patients. The
median age of presentation as postulated by Chauhan, S. C. A., et al. (2015); is 65
years and less than one-third are associated with underlying malignancy. The typical
symptoms of pyometra include uterine enlargement, cramping, vaginal discharge,
acute abdominal pain, and postmenopausal bleeding (Jones, V. A. at al, 1986).
Case Presentation: A 53 year old black African postmenopausal lady of Para 4

Gravida 5 aborta 1 presented to the Oncology Ultrasound Department with a history
of diagnosed cervical carcinoma stage at TNM (T-primary tumour; N-regional lymph
node; M-metastasis) stage 1B revealed on abdominal Multi-Detector Computed
Tomography (MDCT). The CT scan had revealed a cervical cystic mass and dilatation
of left intrahepatic ducts in February 2022. Upon this diagnosis, she received a local
small field irradiation dose to the cervical cancer over ten days after which she was
discharged. She then visited the department in April complaining of drowsiness, loss
of appetite, complaining of non foul smelling discharge and abdominal fullness.
Transabdominal ultrasound findings were of a hypoechoic cervical solid mass of 4.6
cm x 4.01 cm and anechoic endometrial free fluid giving a diagnosis of cervical
carcinoma and hydrometra. She was treated on albothyl suppositories and oral
antibiotics as an outpatient. On 01 August 2022, she presented to the Oncology
Ultrasound Department for ultrasound examination of the pelvis. On physical
examination, her uterus was enlarged about 15 weeks of gestation, she was afebrile,
no fever, complaining of loss of appetite, general body malaise, had foul smelling
purulent discharge and anaemic.
INDICATION
Postmenopausal purulent vaginal discharge.
Date Of Examination: 01 August 2022
PATIENT INFORMATION
Date of Birth: 16 May 1969

Parity: 4
Gravida: 5
Aborta 1
LMP: 8 years ago
Hormonal therapy Nil
Current medication Albothyl suppositories
Radiotherapy treatment Small field irradiation dose for ten days on
cervical cancer
Marital status: Married
Sex: Female
Level of Education: Ordinary Level
EQUIPMENT
Mindray DC-8 Ultrasound machine.
Ultrasound gel.
Standard Gynaecological Transabdominal Scan Protocol documented in appendix A
attached.

 The uterus was enlarged, anteverted, non- gravid, non fibroid and measured 10.60
cm x 6.32 cm x 9.32 cm with an inhomogeneous echotexture. There was an
anechoic fluid collection in the endometrial cavity resulting in marked distention.
 The myometrium was hypoechoic.
 The anechoic endometrial fluid demonstrated posterior enhancement and a
volume of 44.43 cc (4,74x3.11x5.77) cm, thus a dilated fluid filled endometrial
cavity was demonstrated.
 A bulky cervix measuring 5.05 cm x 4.38 cm with an echogenic solid mass was
seen. There was no vascularity seen on color Doppler interrogation.
 Both ovaries were not visualised.
 The adnexae were seen clear of any cystic or solid masses.
 There was no free fluid in the pouch of Douglas and the immediate pelvic region.
 The urinary bladder was partially distended, volume of 94.33 ml (6.18 x 6.23 x
4.68) cm with anechoic urine free of calculi and urinary bladder masses.
COMMENT
 The endometrial free fluid collection of volume 44.43cc is suggestive of
haematometra, hydrometra or pyometra. A provisional diagnosis of endometrial
pyometra was made on the basis of the foul smelling purulent fluid vaginal
discharge seen on physical examination.
 An echogenic cervical mass confirms the previous Multi-Detector Computed
Tomography (MDCT) diagnosis of cervical carcinoma.
 Differential diagnosis: Endometritis, hydrometra or haematometra.
 Recommend cervical dilatation under anaesthesia to obtain pus sample for culture
(laboratory tests).
 Clinical correlation highly advised.
DISCUSSION
Pyometra in postmenopausal females as postulated by Lui, M. W. et al. (2015), is due
to obstruction in drainage of the uterine cavity or a natural drainage impairment
within the cervix, often attributed to a structural process (e.g. cervical stenosis),
benign or malignant pathology, or secondary to radiotherapy. Additionally, urogenital
anomalies, namely atrophic cervicitis, have reportedly contributed to the disease’s
manifestation.
The main causes are malignant diseases of the genital tract and its treatment like
radiotherapy associated cervical stenosis; senile cervicitis, endometritis, cervical
stenosis after surgery, cervical leiomyoma and congenital cervical anomalies
(Mackowiak, P. A. 2006). Similarly, the diagnosis of pyometra in this case was made
basing on the clinical symptom of foul-smelling vaginal discharge and sonographic
appearance of intrauterine fluid collections. In addition, there was an intrauterine
echogenic cervical mass with sonographic features suggestive of cervical carcinoma
presumably causing obstruction in drainage of the uterine cavity often attributed to a
structural process (e.g. cervical stenosis), secondary to radiotherapy.
Characteristically, the symptoms of pyometra include postmenopausal bleeding,

purulent, vaginal discharge and uterine enlargement although they can also be
relatively non-specific. After menopause, when endometrium loses its resistance – not
shed repeatedly, infection which gains entrance to uterus persists as senile
endometritis. The pus which tends to collect in uterus forms pyometra, as cervix is
narrowed by senile change and atrophied myometrium unable to expel it. Ultrasound
is used in most cases for primary diagnoses but sometimes CT, MRI and Doppler
scanning for excluding malignancy like endometrial cancer are necessary modalities.
In the presenting case, abdominal Multi-Detector Computed Tomography (MDCT)

revealed a cervical cystic mass diagnosed as cervical carcinoma stage at TNM (T-
primary tumour; N-regional lymph node; M-metastasis) stage 1B. Following this
staging and diagnosis of the cervical carcinoma, radiation therapy was initiated
together with antibiotics. revealed on abdominal Multi-Detector Computed
Tomography (MDCT). The diagnosis of pyometra should be considered when elderly
women suffer from acute lower abdominal pain. Remarkably, there was an underlying
malignancy, structural deficit, clinical and physical signs/symptoms to account for the
pyometra.
MANAGEMENT
Drainage of pus by repeat dilatations, usually under anaesthesia by putting a Foley’s
catheter/drainage tube followed by curettage under antibiotic is the preferred choice
or route for primary treatment. Thus, the appropriate management of patients with
suspected pyometra should comprise cervical dilatation to drain the pus, together with
antibiotics. Performing hysteroscopy in the presence of pyometra is potentially
dangerous and should be contraindicated because the infected material inside the
uterine cavity may disseminate into the peritoneal cavity via the fallopian tube during
hysteroscopy, resulting in peritonitis and septicaemia(Loffer, F. D. 1995).
CONCLUSION
Pyometra is a collection of purulent fluid within the uterine cavity. Cervical stenosis
most frequently involves the internal os. The acquired causes of cervical stenosis
include infection, neoplasia, and iatrogenic factors (radiation therapy or surgery).
Pyometra is an uncommon, but important gynaecologic condition, because the
incidence of the association with malignant disease is considerable, and spontaneous
rupture can result in significant morbidity and mortality. Dilatation of the cervix and
pus drainage is the treatment of choice, and it is important to rule out the possibility of
cancer and differentiate the malignancy.
Ultrasound has significant clinical utility and Doppler imaging is also beneficial,
particularly in evaluating blood flow changes associated with an inter-current
endometrial cancer. In persistent cases of pyometra, repeat drainage is indicated;
conversely, if the condition is intractable, definitive surgical management is
recommended, particularly when conservative measures have been exhausted or an
underlying malignancy cannot be excluded. Finally, routine surveillance is warranted
to promptly detect or avert substantial haemorrhaging, uterine rupture and peritonitis,
all of which may significantly increase the incidence of patient morbidity and
mortality.
REFERENCES:
1. Chauhan, S. C. A., Sharma, L. C. M. M., and Banerjee, B. J. K. (2015):

Spontaneous Perforation Of Pyometra: a Rare Cause Of Diffuse Peritonitis. Med J
Armed Forces India. 2015;71:192–3.
2. Loffer, F. D. (1995): Contraindications And Complications Of Hysteroscopy.
Obstet Gynecol Clin North Am 1995; 22: 445–55.
3. Lui, M. W., Cheung, V. Y. and Pun, T. C. (2015): Clinical Significance Of
Pyometra. J Reprod Med 2015; 60: 329-32.
4. Mackowiak, P. A. (2006): An Elderly Woman With Pain And Fever. CID.
2006:1218–9.
CASE STUDY-POLYCYSTIC OVARIES/ OVARIAN SYDROME
INTRODUCTION
Polycystic Ovarian Syndrome (PCOS) is a physiological disorder that causes many

negative effects involving a variety of systems in the body, such as the endocrine,
metabolic, psychological, and reproductive systems. It can be defined as a complex
endocrine (hyperandrogenic) disease of women of premenopausal, reproductive and
postmenopausal ages with variable prevalence rates and clinical manifestations.
PCOS is the most common endocrine disorder among women of reproductive age,
with symptoms of PCOS being seen in pre-pubertal girls, in some cases, and post-
menopausal women, in many instances (Thomson et al., 2011). Its pathogenesis is
multifactorial and complex often associated with insulin resistance.
The aetiology of this syndrome remains largely unknown, but mounting evidence
suggests that PCOS might be a complex multigenic disorder with strong epigenetic
and environmental influences, including diet and lifestyle factors. It is frequently
associated with abdominal adiposity, insulin resistance, obesity, metabolic disorders
and cardiovascular risk factors. PCOS is defined by a combination of signs and
symptoms of androgen excess and ovarian dysfunction in the absence of other specific
diagnoses. The principal features are obesity, irregular or absence of menstruation,
acne, difficulty in conceiving, excessive amounts of male hormones and excessive
hair growth.
The diagnosis and treatment of PCOS are not complicated, requiring only the
judicious application of a few well-standardized diagnostic methods and appropriate
therapeutic approaches addressing hyperandrogenism, the consequences of ovarian
dysfunction and the associated metabolic disorders. Accordingly, guidelines from the
Endocrine Society recommend using the Rotterdam Criteria for the diagnosis of
PCOS. The Rotterdam Criteria mandate the presence of 2 of the following three
findings: hyperandrogenism-(either clinically by skin manifestations of androgen
excess or hyperandrogenemia - high testosterone in a blood test), ovulatory
dysfunction - (oligo / anovulation), and polycystic ovaries on ultrasound; plus the
exclusion of other diagnoses that could result in hyperandrogenism or ovulatory
dysfunction such as congenital adrenal hyperplasia (CAH), androgen-secreting
tumours, Cushing syndrome, thyroid dysfunction, and hyperprolactinemia.
Case Presentation: A 24 year old morbidly obese married black African lady of Para
0 Gravida 0 aborta 0 presented to the Ultrasound Department for a pelvic
examination to rule out polycystic ovaries. Her history revealed that she was not
having a period for the last six months and had irregular menses since menarche. Her
menarche was at 13 years and her periods have been irregular since then. The patient
stated that during her adolescence, her periods would vary with change of
environment and that the last time she had a period she had consulted a faith healer
who gave her some Holy water. She only had a period for two months and since then,
she assumed to be pregnant since she had missed her periods. She also has been trying
to conceive for the last year and a half without success. She has noticed a significant
weight gain (98 kg) over the last few months or so and was convinced she was
pregnant even though all pregnancy tests have come back negative.
She denied any change in her voice or increase in the size of her muscles. She has
been morbidly obese since she was a young teenager. She denied any headaches,
blurred vision, or discharge from her nipples. She also denied any hyper/hypothyroid
symptoms. She has never had any surgery and has never conceived, despite several
years of trying. She is not currently taking any medication and has never used any
form of contraception.
On examination, she was clearly not hirsute (Ferriman-Gallowey score of 0),

especially in the chin and mid abdominal regions. Her height was 165 cm giving a
BMI was 27.22. Her pelvic exam was unremarkable, including no evidence for
clitoromegaly, but her uterus and adnexa were very difficult to assess secondary to the
patient's morbid obesity. The rest of her physical exam was unremarkable. Blood
samples for serum TSH and serum prolactin were taken for laboratory tests.
INDICATION
Pelvic examination to rule out polycystic ovaries and evaluation of irregular menses.
Date Of Examination: 07 September 2022
PATIENT INFORMATION
Date of Birth: 23 June 1998

Parity: 0
Gravida: 0
Aborta 0
LMP: 6 months ago though mostly irregular
Menarche 13 years
Hormonal therapy Nil
Current medication Nil
Marital status: Married
Sex: Female
Level of Education: Tertiary Level
EQUIPMENT
Mindray DP 50 Ultrasound machine.
Ultrasound gel.

Standard Gynaecological Transabdominal Scan Protocol documented in appendix A
attached.

 The uterus was anteverted, non-gravid and non-fibroid with a homogeneous
echotexture. It measured (6.18 x 2.27 x 4.85) cm. It had a regular shape, normal
size and outline.
 The endometrium appeared normal in shape and had a thin echo complex
measuring 0.39 cm in antero-posterior (AP) diameter.
 The cervix had a normal size, shape and echotexture. The cervical size was
assessed subjectively.
 The right ovary appeared enlarged with an area of (4.69 x 3.21) 11.93 square
centimetres and a volume of 24.62 cubic centimetres with an oval shape and
regular outline. There were multiple similar sized small peripheral follicles. The
peripheral distribution of follicles gave a “string of pearls” appearance. The
stroma was echogenic relative to the peripheral follicles and there was no
dominant follicle seen. The number of follicles was in excess of 14.
 The left ovary was larger than the right ovary with an area of (4.15 x 4.26) 12.69
square centimetres and a volume of 33.26 cubic centimetres. It had numerous
peripherally distributed follicles of size ranging between 0.23 to 0.48 cm without
a dominant follicle. The stroma was hypoechoic relative to the anechoic follicles.
 There were no adnexal solid or cystic masses seen in both ovaries.
 There was no free fluid collection in the pouch of Douglas.
 The urinary bladder was overly distended with anechoic urine and showed a thin
smooth regular echogenic wall. No urinary bladder wall masses or calculi were
seen. The urinary bladder emptied completely with no urine retention on post
micturition imaging.
COMMENT
 Normal sonographic findings of the uterus, endometrium and cervix were noted.
 There was bilateral enlargement of both ovaries with numerous small similar
sized and peripherally distributed anechoic follicles without a dominant follicle.
 Relatively echogenic right ovarian stroma.
 The sonographic appearance of both ovaries were consistent with polycystic
ovaries.
Differential diagnosis: Bilateral multicystic ovaries; (obesity, hypothyroidism,
hyperprolactinemia as the causes of anovulation).
 Recommend a progesterone challenge test.
 Correlate with clinical and laboratory findings as per “Rotterdam Criteria, for
diagnosis of POCS.
DISCUSSION
Polycystic ovarian syndrome (PCOS) is a common endocrinopathy with many clinical
manifestations. The effects on women’s lives start at puberty and can last throughout
her lifetime. Women frequently experience anovulatory menstrual cycles, infertility,
hirsutism, obesity and increased risk of diabetes mellitus, hypertension, lipid
abnormalities, and metabolic syndrome. PCOS is a heterogeneous disorder, and a
diagnosis of exclusion. In general, women afflicted will have menstrual irregularities,
ultrasound findings of abnormal ovarian size and morphology, and clinical or
laboratory evidence of hyperandrogenism.
While there are a number of definitions of PCOS, the Rotterdam consensus is the
most widely accepted across Europe, Asia and Australia and was the definition used
for the guideline. It encompasses the National Institutes of Health definition, which
generally describes women with a more severe form of PCOS and requires the
presence of both hyperandrogenism and oligo/anovulation. The Rotterdam Criteria
require the presence of two of the following: oligo/anovulation, hyperandrogenism or
polycystic ovaries on ultrasound; (Revised 2003 consensus on diagnostic criteria). In
this regard, it is therefore paramount to note that other aetiologies must be excluded
such as congenital adrenal hyperplasia, androgen secreting tumours, Cushing
syndrome, thyroid dysfunction and hyperprolactinaemia. Based on the Rotterdam
Criteria, the patient in this scenario would be diagnosed with PCOS as the ultrasound,
and clinical features of the disorder were present.
Pathophysiology
The pathophysiology of PCOS encompasses inherent ovarian dysfunction that is
strongly influenced by external factors, such as disturbances of the hypothalamic-
pituitary-ovarian axis and hyperinsulinaemia. Exaggerated gonadotrophin releasing
hormone (GnRH) pulsatility results in hypersecretion of luteinising hormone (LH),
which has effects both on ovarian androgen production and oocyte development.
Disturbed ovarian-pituitary and hypothalamic feedback accentuates the gonadotrophin
abnormalities. Hyperinsulinaemia is secondary both to insulin resistance at the
periphery and to abnormal pancreatic beta cell function. PCOS runs in families and a
number of genetic abnormalities appear to result in features of the syndrome and
account for the heterogeneity of the symptoms. Environmental influences, such as
nutrition and lifestyle, further influence expression of the syndrome. No one factor
fully accounts for PCOS abnormalities; thus in the presenting case, although it is an
abnormality of both the reproductive and endocrine (metabolic) systems; the patient’s
disorder can be attributed to insulins resistance/ hyperinsulinemis, disorders of
luteinizing hormone/follicle stimulating hormone release, decrease in sex hormone-
binding globulin (SHBG) production, increased ovarian androgen production which
all components can lead to anovulation causing PCOS.
The aetiology of polycystic ovary syndrome is poorly understood, and is thought to

be multifactorial in origin.The two most common hormonal abnormalities present in
PCOS are: Excess luteinising hormone (LH) – produced by the anterior pituitary
gland in response to an increased GnRH pulse frequency which stimulates ovarian
production of androgens; and Insulin resistance – resulting in high levels of insulin
secretion that suppresses hepatic production of sex hormone binding globulin
(SHBG), resulting in higher levels of free circulating androgens. Despite the high
levels of LH, the increased circulating androgens suppress the LH surge (which is
required for ovulation to occur). Follicles develop within the ovary, but are arrested at
an early stage (due to the disturbed ovarian function) – and they remain visible as
“cysts” within the ovary.
According to Carvalho, L. M. L. et al, (2018), citing Marciniak, A. et al,; Sala

Elpidio, L. N. et al,; and Shorakae, S. at al,; (2018), postulated that the causes for this
dysregulation include insulin excess, which is known to sensitize the ovary to LH by
interfering with the process of homologous desensitization to LH in the normal
ovulation cycle as well as an intrinsic imbalance among intraovarian regulatory
systems. Theca cells in PCOS have over-expression of most steroidogenic enzymes
and proteins involved in androgen synthesis, which suggests a prominent abnormality
at the level and activity of steroidogenic enzymes. Granulosa cells prematurely
luteinise primarily as a result of androgen and insulin excess.
Androgen excess enhances the initial recruitment of primordial follicles into the
growth pool. Simultaneously, it initiates premature luteinisation, which impairs the
selection of the dominant follicle. This results in classical PCOS histopathologic and
gross anatomic changes that constitute Polycystic Ovarian Morphology (PCOM).
PCOS is perpetuated by increased LH, but it is not caused by it. LH excess is common
and is necessary for the expression of gonadal steroidogenic enzymes and sex
hormone secretion but is less likely to be the primary cause of ovarian androgen
excess because of LH-induced desensitization of theca cells.
Abundant literature note that nearly one-half of patients with functional ovarian
hyperandrogenism have an abnormal degree of insulin-resistant hyperinsulinism,
which acts on theca cell, increasing steroidogenesis and prematurely luteinises
granulosa cells, and stimulates fat accumulation. Hyperandrogenemia provokes LH
excess, which then acts on both theca and luteinised granulosa sustaining cycle.
Ovarian hormonal dysregulation alters the pulsatile gonadotropin-releasing hormone

(GnRH) release, potentially leading to a relative increase in LH versus FSH
biosynthesis and secretion. LH stimulates ovarian androgen production, while the
relative decrease of FSH prevents adequate stimulation of aromatase activity within
the granulosa cells, decreasing androgen conversion to the potent oestrogen
estradiol. This becomes a self-perpetuating non-cyclic hormonal pattern.
Elevated serum androgens are converted in the periphery to oestrogens, mostly

oestrone. As conversion occurs primarily in the stromal cells of adipose tissue,
oestrogen production will be augmented in obese PCOS patients. This conversion
results in chronic feedback at the hypothalamus and pituitary gland, in contrast to the
normal fluctuations in feedback observed in the presence of a growing follicle and
rapidly changing estradiol levels. Unopposed oestrogen stimulation of the
endometrium may lead to endometrial hyperplasia.
Evaluation
Most society guidelines have accepted that diagnosis of PCOS; most meet two out of
three criteria: chronic anovulation, clinical or biological hyperandrogenism, and
polycystic ovaries morphology in the absence of any other pathology. These clinical
features are part of the Rotterdam Criteria. The National Institute of Health criteria
also requires clinical or biochemical hyperandrogenism and oligo or anovulation. The
American Excess PCOS Society requires hyperandrogenism with one of two of the
remaining criteria.
Xie, J., et., al; (2018); asserts that the disorders mimicking the clinical features of
PCOS should be excluded. These include thyroid disease, hyperprolactinemia, and
non-classic congenital adrenal hyperplasia with 21-hydroxylase deficiency, for which
measurement of serum 17-hydroxyprogesterone (17-OHP) should be done, which
may require further testing with adrenocorticotropin stimulation test.
Chronic Anovulation: The cycle length of more 35 days suggest chronic
anovulation, but cycle length between 32 to 35-36 day needs to be assessed for
ovulatory dysfunction. The threshold for oligomenorrhea is 35 days cycles in adults
and 40 days in adolescents. A patient with cycles shorter than 35 days can be assessed
by measuring progesterone levels in the mid-luteal phase (days 20 to 21). Implications
of ovulatory dysfunction include infertility, endometrial hyperplasia, and endometrial
cancer. In the presenting case the patient had worries with infertility since her
menstrual history since menarche was sporadic and irregular and then, she had been
trying to conceive for the more than a year without success.
Hyperandrogenism: Clinical hyperandrogenism is diagnosed in adult women with

hirsutism, alopecia, and acne, and these are a good substitute for biochemical
hyperandrogenism. However, adolescent-only hirsutism should be considered as a
substitute for biochemical hyperandrogenism. Hair loss patterns are variable, typically
in a vertex, crown, or diffuse pattern. Women with more severe hyperandrogenemia
may suffer from bi-temporal hair loss and loss of the frontal hairline.
Hirsutism is defined as coarse, dark, terminal hairs distributed in a male pattern. Signs
of virilization such as increased muscle mass, decreased breast size, deepening of the
voice, and clitoromegaly are not typical of PCOS. Virilization reflects higher
androgen levels, and further investigation should be done; the clinician should have
higher suspicion for an androgen-producing tumour of the ovary or the adrenal gland.
Free testosterone levels are more sensitive than the measurement of total testosterone
for establishing the existence of androgen excess.
The patient in this case denied any change in her voice or increase in the size of her
muscles; any headaches, blurred vision, or discharge from her nipples. She also
denied any hyper/hypothyroid symptoms. She has never had any surgery and has
never conceived, despite several years of trying. She is not currently taking any
medication and has never used any form of contraception. On examination, she was
clearly not hirsute (Ferriman-Gallowey score of 0), especially in the chin and mid
abdominal regions and had no evidence for clitoromegaly.
Polycystic Ovaries Morphology: Ovarian morphology assessment is more accurate
when done by transvaginal ultrasound. New ultrasound machines allow the diagnosis
of PCOM in patients having at least 25 small follicles (2 mm to 9 mm) in the whole
ovary. Ovarian size at 10 ml remains the normal size cut-off. Rotterdam criteria
indicate PCOM by the presence of at least 12 follicles measuring 2 mm to 9 mm in
the whole ovary or increased ovarian size more than 10 ml. Ultrasound technology
has advanced and can improve the diagnosis of PCOS. In the current scenario, the
patient’s transabdominal ultrasound revealed bilateral enlargement of both ovaries
with numerous small similar sized and peripherally distributed anechoic follicles
without a dominant follicle and relatively echogenic right ovarian stroma; giving
sonographic appearance of both ovaries consistent with polycystic ovarian
morphology.
Characteristics of PCOS according to the assertion of (McCance & Huether, 2019),
usually present during puberty and include obesity, menstrual disturbances,
oligomenorrhea, amenorrhoea, hyperandrogenism, infertility, and some women
maybe asymptomatic. The majority of these PCOS features were present in the
patient in question. Other manifestations of PCOS which may be excluded as the
guidelines of Revised 2003 consensus on diagnostic criteria like cardiovascular
disease hypertension, dyslipidemia, diabetes mellitus and hormones disturbances such
as increases in LH, insulin, androgens and prolactin were not proven by the laboratory
test results for this patient by the time the report was produced. Nonetheless, a
diagnosis of the patient’s disorder was already made based in the diagnostic criteria.
Management
Management of PCOS requires identification and management of current symptoms,
attention to fertility and emotional concerns, as well as preventive activities to
minimise the risk of future associated health problems. The national guideline
highlights the key role of obesity in PCOS. Studies consistently show a higher
prevalence of PCOS in women who are overweight and obese, and up to 30% of s
women who had a body mass index (BMI) >30 kg/m2 met PCOS diagnostic criteria
(Boyle, J. A,. et al 2012). Women with PCOS also have a higher rate of weight gain
than those without PCOS – about 1–2 kg/year.7 A lifestyle program that addresses a
healthy diet with caloric restriction, behaviour change support and exercise to aid in
weight loss and prevention of future weight gain is the best first line treatment for
PCOS.4 Even a small amount of weight loss (5%) can help restore menstrual cycle
regularity and ovulation, assist mental wellbeing, halve the risk of diabetes in high
risk groups and help prevent future cardiometabolic risk.8–11
No evidence supports any particular exercise regimen as best for women with PCOS.
General recommendations include 150 minutes of exercise weekly with 90 minutes of
this exercise being aerobic activity at moderate to high intensity.4 Lifestyle with diet
and exercise should always be a core part of management in addition to other
treatment measures. Health coaching principles with appropriate education, risk
perception and patient driven goal setting may assist with motivation and support in
behaviour change. A team approach may also be useful. Anxiety, depression and body
image disorders may also impact on the woman’s ability to take-up lifestyle advice
and these should also be addressed.4
Reference
Boyle JA, Cunningham J, O’Dea K, Dunbar T, Norman RJ. Prevalence of polycystic
ovary syndrome in a sample of Indigenous women in Darwin, Australia. Med J Aust
2012;196:62–6. Search PubMed
Revised 2003 consensus on diagnostic criteria and long-term health risks related to
polycystic ovary syndrome. Fertil Steril 2004;81:19–25. Search PubMed.
Carvalho LML, Dos Reis FM, Candido AL, Nunes FFC, Ferreira CN, Gomes KB.
Polycystic Ovary Syndrome as a systemic disease with multiple molecular pathways:
a narrative review. Endocr Regul. 2018 Oct 01;52(4):208-221. [PubMed]
11.
McCance, S. & Huether, S.E. (2019). Patholophysiology: The biologic basis for
disease in adults and children(8th ed.). St. Louis, Missouri: Mosby, an affiliate of
Elsevier Inc.
Marciniak A, Lejman-Larysz K, Nawrocka-Rutko wska J, Brodowska A, Songin D.
[Polycystic ovary syndrome - current state of knowledge]. Pol Merkur Lekarski. 2018
Jun 27;44(264):296-301. [PubMed]
12.
Sala Elpidio LN, de Alencar JB, Tsuneto PY, Alves HV, Trento Toretta M, It Taura
SK, Laguila Visentainer JE, Sell AM. Killer-cell immunoglobulin-like receptors
associated with polycystic ovary syndrome. J Reprod Immunol. 2018 Nov;130:1-
6. [PubMed]
13.
Shorakae S, Ranasinha S, Abell S, Lambert G, Lambert E, de Courten B, Teede H.
Inter-related effects of insulin resistance, hyperandrogenism, sympathetic dysfunction
and chronic inflammation in PCOS. Clin Endocrinol (Oxf). 2018 Nov;89(5):628-
633. [PubMed]
Xie J, Burstein F, Garad R, Teede HJ, Boyle JA. Personalized Mobile Tool AskPCOS
Delivering Evidence-Based Quality Information about Polycystic Ovary
Syndrome. Semin Reprod Med. 2018 Jan;36(1):66-72. [PubMed] [Reference list]

Case Study

Uploaded by

Copyright:

Available Formats

Case Study

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Case Study

Uploaded by

Copyright:

Available Formats

CASE STUDY-UTERINE FIBROID/LEIOMYOMA IN PREGNANCY

Uterine fibroids or leiomyomas represent benign hormone-dependent tumours of

It is known that uterine fibroids, especially multiple, intramural or sub-mucosal, are

PATIENT PREPARATION, PATIENT CARE AND PROTOCOL

(a) (b) (c) (d)

 Therefore the average EGA was 7 weeks 5 days

Uterine Fibroid And Pregnancy

Possible Causes of Fibroids

In order to maintain productiveness and menstrual function in young female patients,

1. Chudleigh T and Thilaganathan B. (2004): Obstetric Ultrasound: How, Why

Uterine fibroids, otherwise known as myomatous or leiomyoma, are benign,

Several factors have been implicated in the etiology of fibroids. Epidemiological

Etiology and Pathophysiology

The role of ovarian steroid hormones in the pathogenesis of uterine fibroids is

ULTRASOUND FEATURES OF UTERINE FIBROIDS

In order to maintain productiveness and menstrual function in young female patients,

1. Chudleigh T and Thilaganathan B, 2004. Obstetric Ultrasound: How, Why and

A molar pregnancy also known as hydatidiform mole is a rare complication of

Complete molar pregnancy usually occurs when an egg without maternal

Date Of Examination: 15 August 2022

Date of Birth: 16 December 1994

PATIENT PREPARATION, PATIENT CARE AND PROTOCOL

ULTRASOUND FEATURES OF MOLAR PREGNANCY

Transabdominal ultrasound revealed an anteverted, non- gravid(with no visible GS)

Suction curettage is the optimal method of evacuation, regardless of uterine size, in

Hysterectomy is an alternative in patients who do not wish to maintain fertility or who

In addition, final follow-up requires serial measurements of serum hCG every 1 to 2

The American College of Obstetricians and Gynaecologists has recommended that

1. Fowler, D. J., Lindsay, I. and Seckl, M. J. (2006). Routine pre-evacuation

Pyometra is an uncommon result of endometritis. The diagnosis of pyometra is made

Case Presentation: A 53 year old black African postmenopausal lady of Para 4

Date of Birth: 16 May 1969

OBSERVATIONS AND FINDINGS

Characteristically, the symptoms of pyometra include postmenopausal bleeding,

In the presenting case, abdominal Multi-Detector Computed Tomography (MDCT)

1. Chauhan, S. C. A., Sharma, L. C. M. M., and Banerjee, B. J. K. (2015):

Polycystic Ovarian Syndrome (PCOS) is a physiological disorder that causes many

On examination, she was clearly not hirsute (Ferriman-Gallowey score of 0),

Date of Birth: 23 June 1998

PATIENT PREPARATION, PATIENT CARE AND PROTOCOL

OBSERVATIONS AND FINDINGS

The aetiology of polycystic ovary syndrome is poorly understood, and is thought to

According to Carvalho, L. M. L. et al, (2018), citing Marciniak, A. et al,; Sala

Ovarian hormonal dysregulation alters the pulsatile gonadotropin-releasing hormone

Elevated serum androgens are converted in the periphery to oestrogens, mostly

Hyperandrogenism: Clinical hyperandrogenism is diagnosed in adult women with

You might also like