1. health and fitness
2. disease
3. infertility

CLINICAL
guided learning
Diagnosis and treatment of
polycystic ovarian syndrome
Aherne, S.A. (2004) Polycystic ovary
syndrome. Nursing Standard;
18: 26, 40–44.
Balen, A. (2000) Surgical management
of polycystic ovary syndrome: pros and
cons. The Obstetrician and
Gynaecologist; 12: 3, 17–20.
Balen, A. (1995) The polycystic ovary
syndrome. Maternal and Child Health;
20: 2, 58–61.
Campbell, I.M., Poirier, B.W. (2000)
Polycystic ovary syndrome: a case
presentation. Clinical Excellence for
Nurse Practitioners; 4: 6, 341–344.
Edwards, M. (1999) Know the symptoms
and the risks of PCOS. Practice Nurse;
18: 8, 502–506.
Polycystic ovarian syndrome (PCOS) is a complex hormonal disturbance with numerous implications for general
health and well-being (McKittrick, 2002). It is the most
common endocrine gland disorder in women of reproductive age (Lockwood, 1997) and has a prevalence of
5–10 per cent in this group (Hill, 2003). However, many
women remain undiagnosed or are misdiagnosed as
having other conditions such as premenstrual syndrome
(Harris and Carey, 2000; Raisbeck, 1999).
Normal physiology
According to Polson et al (1988), although about 20 per
cent of all women are found to have polycystic ovaries
on ultrasound, only 10–20 per cent of these develop full
PCOS. The two conditions are occasionally referred to collectively as PCO/S (Harris and Carey, 2000).
To appreciate the complexity of PCOS, it is important to
understand the menstrual cycle and the hormones
involved. A normal 28-day cycle commences with the
onset of menstruation, coinciding with the development
Learning objectives
Each week Nursing Times publishes a guided learning article with reflection
points to help you with your CPD. After reading the article you should be able to:
40
l
Understand the implications of polycystic ovarian syndrome;
l
Be familiar with the symptoms associated with the condition and the diagnostic process;
l
Be familiar with the treatments available to treat the symptoms of PCOS;
l
Understand the implications of PCOS for nursing practice.
of a dominant cyst (a follicle) within the ovary (Kelley,
2003). During the cycle’s first (follicular) phase, the
hypothalamus sends gonadotrophin-releasing hormone
(GnRH) to the pituitary gland, triggering it to release low
levels of follicle-stimulating hormone (FSH).
To produce oestrogen, follicles require a small amount
of luteinising hormone (LH). This causes the thecal cells
(ovary cells directly surrounding the follicle) to manufacture testosterone, which is transported to the cells on the
inside of the follicle (granulosa cells) (Harris and Carey,
2000). There, an enzyme called aromatase converts testosterone into oestrogen, and as the follicle increases in
size stimulated by FSH, oestrogen production increases
(Harris and Carey, 2000). This rise in oestrogen levels,
especially late in the follicular phase, boosts the release
of LH and FSH from the anterior pituitary in a positive
feedback loop. As a result, LH and FSH secretion increases
rapidly prior to ovulation (Seeley et al, 2003).
The sharp rise in LH secretion is not only due to the
direct effect of oestrogen on the anterior pituitary but also
to the increase in secretion of GnRH by the hypothalamus (Tortora and Anagnostakos, 1990). On the 14th day
of the cycle, ovulation is initiated by this LH surge, causing the ovulated follicle to become the corpus luteum.
Shortly after ovulation, in the luteal phase of the cycle,
oestrogen production decreases and progesterone increases as the granulosa cells change to corpus luteum
cells (Seeley et al, 2003). Progesterone prepares the endo­
metrium for implantation of the ovum in the event of
fertilisation (Kelley, 2003).
The increase in progesterone has a negative feedback
effect on GnRH release from the hypothalamus, resulting
in a decrease in LH and FSH release from the anterior
pituitary (Seeley et al, 2003). On day 24 or 25, before the
end of the cycle on day 28, the corpus luteum regresses,
leading to a fall in progesterone levels and a deterioration
of the endometrial lining, which results in menstruation.
The condition
PCOS is a complex, heterogeneous disorder involving a
combination of abnormalities associated with PCO
(Aherne, 2004). However, there remains a degree of uncertainty about its aetiology (Hopkinson et al, 1998).
There is some evidence to suggest autosomal genetic
transmission, with strong familial clustering (Hopkinson
et al, 1998). McKittrick (2002) asserts that women with
PCOS often have both male and female relatives with
adult-onset diabetes, obesity, elevated blood triglycerides and high blood pressure, and female relatives with
infertility, hirsutism and menstrual problems.
NT 18 January 2005 Vol 101 No 3 www.nursingtimes.net
SPL
References
AUTHOR Ann Elaine Jones, BSc, RGN, is tutor in clinical skills, University of Wales Swansea, School of Health
Science, Carmarthen.
ABSTRACT Jones, A.E. (2005) Diagnosis and treatment of polycystic ovarian syndrome. Nursing Times;
101: 3, 40–43.
Polycystic ovarian syndrome is a hormonal disturbance
that results in a collection of symptoms and has wideranging health implications. There is evidence that it
may run in families, and it is associated with the development of type 2 diabetes and recurrent miscarriage.
Diagnosis involves eliminating other potential conditions, while treatment aims to manage individual
symptoms rather than provide a cure.
keywords n Polycystic ovarian syndrome n Fertility n Women’s health
Box 1. Clinical Features (Aherne, 2004)
HYPERANDROGENISM – clinically characterised by:
l Hirsutism;
l Acne;
l Oily
skin;
l Virilisation (development of secondary male sex
characteristics);
l Anovulation.
ANOVULATION – manifested clinically as:
l Menstrual disturbance, involving dysfunctional
uterine bleeding;
l Oligomenorrhoea
(infrequent/diminished
menses);
l Primary
amenorrhoea (never had menses);
l Secondary amenorrhoea (absence of menses for
more than three months);
l And/or
infertility.
METABOLIC DISTURBANCES:
l Dyslipidaemia;
l Cardiovascular
risk;
l Hyperinsulinaemia;
l Insulin
resistance and risk of diabetes.
It may be that a gene or series of genes renders the
ovaries susceptible to the insulin-mediated stimulation
of androgen secretion, while blocking maturation of the
follicles. This genetic predisposition may be expressed as
premature balding in men (Hopkinson et al, 1998).
Kelley (2003) maintains that PCOS is a much more
complex disorder, and that there may be two types: one
primarily LH dependent and the other primarily insulin dependent. In LH-dependent PCOS, normal ovarian function
is dependent on appropriate signals from the FSH and LH
secreted from the pituitary gland (McKittrick, 2002).
PCOS is characterised by hyperstimulation of the pituitary by LH (McKittrick, 2002). This constant stimulation of
the ovary results in anovulation, multiple cysts and excess androgen output (Kelley, 2003). Harris and Carey
(2000) maintain that an elevated level of LH can be a
useful marker for predicting women who are at risk of
miscarriage. Regan (1990) demonstrated that 67 per
cent of women with an elevated LH miscarried, compared with seven per cent of those with a normal level
of LH. Following on from this, over 80 per cent of women
presenting with recurrent miscarriage are recognised as
having polycystic ovaries (Harris and Carey, 2000).
It has been suggested that primarily insulin-dependent
PCOS is the product of a metabolic state of insulin resistance in which it is difficult to transfer glucose into the
NT 18 January 2005 Vol 101 No 3 www.nursingtimes.net
cells (Kelley, 2003). This results in increased blood glucose, which signals for further secretion of insulin, leading to hyperinsulinaemia. Insulin, in combination with
LH, stimulates an increase in the manufacture of testosterone by the ovaries and decreases the level of sex
hormone-binding globulin (SHBG), resulting in more free
testosterone and a potential exacerbation of symptoms
(Harris and Carey, 2000).
Diagnosis
Hill (2003) asserts that a diagnosis of PCOS should be
considered when women present with symptoms such
as menstrual cycle dysfunction, infertility and hirsutism.
Due to the syndrome’s heterogeneous nature the development of a diagnostic category has proven difficult
(Hill, 2003), but Marantides (1997) maintains that diagnosis should commence with a detailed history and
physical examination, focusing on the elimination of
other possible differential diagnoses.
History
Initially, a brief review of symptoms should be completed,
establishing any contributory chronic illnesses, abnormalities and medication history (Marantides, 1997). If
one of the more common symptoms of PCOS is absent or
menstrual flow is decreased, a thorough menstrual history is vital. This should include information on age of
menarche, if and at what age periods regulated, duration of menstrual cycle, flow volume and duration, and
any change apparent over time (Miller, 2002).
An accurate menstrual history can be obtained by asking the patient to keep a diary noting commencement of
menstruation and quantity of flow each day. Further
information regarding reproductive history is important,
including contraception, number of pregnancies, miscarriages and terminations (Miller, 2002). Symptoms of
excess androgens, such as abnormal hair growth and distribution, voice changes, frontal balding and clitorimegaly
should be explored (Marantides, 1997). The hirsutism of
PCOS is characterised by coarse hair on the upper lip,
chin, sideburn area, periareolar area, chest, lower abdomen in the midline and inner thighs (Miller, 2002).
A careful medical history is vital, as many drugs have
been associated with hirsutism including antiepileptics
such as phenytoin and sodium valproate (Hill, 2003).
Acanthosis nigricans (a skin disorder that causes lightbrown-to-black, velvety, rough areas or increased skin
markings) mainly in the axilla and other body folds is an
indication of PCOS and suggestive of significant insulin
resistance. Screening should be undertaken for diabetes,
including excessive thirst, hunger, urination, along with
information regarding fertility and any history of weight
gain or acne (Miller, 2002).
Enquiries into family history are also vital: a woman
whose mother or sister has PCOS is at highest risk. Family history of hypertension, diabetes, obesity and early
coronary artery disease should also be explored, as these
may be the only available historical clues (Miller, 2002).
References
Harris, C., Carey, A. (2000) PCOS:
A Woman’s Guide to Dealing with
Polycystic Ovary Syndrome.
London: Thorsons.
Harris, C., Cheung, T. (2002) PCOS Diet
Book: How You Can Use the Nutritional
Approach to Deal with Polycystic Ovary
Syndrome. London: Thorsons.
Hill, K. (2003) Update: the pathogenesis
and treatment of PCOS. Nurse
Practitioner; 28: 7, 8–17.
Hopkinson, Z.E.C. et al (1998) Polycystic
ovarian syndrome: the metabolic
syndrome comes to gynaecology. British
Medical Journal; 317: 329–332.
Kelley, L.S. (2003) Polycystic ovarian
syndrome a challenge for occupational
health nursing. American Association of
Occupational Health Nurses Journal;
51: 1, 23–27.
Lockwood, G. (1997) Polycystic ovarian
syndrome diagnosis and management.
Practice Nursing; 8: 1, 32–34.
Marantides, D. (1997) Management of
polycystic ovary syndrome. Nurse Practitioner; 22: 12, 34–41.
McKittrick, M. (2002) Diet and polycystic
ovary syndrome. Nutrition Today;
37: 2, 63–69.
This article has been double-blind
peer-reviewed.
For related articles on this subject
and links to relevant websites see
www.nursingtimes.net
41
Guided learning
References
Miller, K.E. (2002) A new look at
polycystic ovary syndrome. Family
Practice Recertification; 24: 9, 51–58.
Munson, B.L. (2002) Myths and facts
about polycystic ovarian syndrome.
Nursing; 32: 11, 78.
Polson, D.W. et al (1988) Polycystic
ovaries: a common finding in normal
women. The Lancet; 1: 8590, 870–872.
Raisbeck, E. (1999) A sympathetic
approach to PCOS sufferers. Practice
Nurse; 18: 4, 212–216.
Regan, L. et al (1990) Hypersecretion of
LH, infertility and spontaneous abortion.
Lancet; 336: 8724, 1141–1144.
Rosevear, S.K. (2002) Handbook of
Gynaecology Management. Oxford:
Blackwell Science.
Seeley, R.R. et al (2003) Anatomy and
Physiology. London: McGraw Hill.
Tortora, G.J., Anagnostakos, N.P. (1990)
Principles of Anatomy and Physiology.
New York, NY: HarperCollins.
Pelvic and physical examination
A physical examination measuring blood pressure,
weight and height should be completed. A routine pelvic
and general physical examination should also be conducted, noting the presence of secondary sex characteristics, along with palpation of the thyroid gland for
masses or enlargement. The ovaries and adnexae should
be palpated for signs of enlargement and the presence
of any tumours or cysts, both of which suggest PCOS
(Marantides, 1997).
Kelley (2003) maintains PCOS is a diagnosis of exclusion,
requiring the presence of hirsutism, evidence of ovarian
dysfunction and obesity. These features usually appear at
adolescence and deteriorate over time.
Laboratory studies
Further diagnostic information can be obtained through
laboratory measurement of FSH, LH, thyroid-stimulating
hormone, prolactin, dehydroepiandrosterone and testosterone levels to ascertain the exact hormonal imbalance
(Munson, 2002). Total cholesterol and high-density lipoprotein cholesterol levels should also be obtained as a
baseline (Campbell and Poirier, 2000).
However, establishing a diagnosis of PCOS insulin resistance is more problematic and can only be gauged
from clinical signs of PCOS and impaired glucose metabolism, which is demonstrated in the laboratory by a fasting glucose level of 110–125mg/dL, impaired two-hour
glucose tolerance test (GTT) of 140–199mg/dL, and fasting insulin ratio of <4.5 (Kelley, 2003).
Ultrasonography
Ultrasonography can be helpful in establishing the diagnosis of PCOS. A finding of eight or more discrete ovarian
follicles smaller than 10mm in diameter is suggestive of
the syndrome (Miller, 2002). Follicles are usually on the
periphery of the ovary, arrayed around an enlarged hyperechogenic ovarian stroma (Miller 2002). Diagnosis of
PCOS is therefore preferable when there are the associated symptoms, namely irregularity of the menstrual
cycle, hyperandrogenisation, obesity or raised serum LH
and testosterone in addition to ultrasound findings of
polycystic ovaries (Balen, 1995).
Guided reflection
Use the following points to write a reflection for your PREP portfolio:
42
l
Outline your area of expertise and why you read this article;
l
Explain the implications of PCOS for the health and well-being of women;
l
Summarise the symptoms of PCOS and the diagnostic process;
l
Summarise the treatment available;
l
Explain how the information in this article will help you in your future practice.
Signs and symptoms
Aherne (2004) states that the major clinical features pertaining to PCOS can be divided into three components:
l Hyperandrogenism – characterised by elevated levels
of serum androgen;
l Anovulation;
l Metabolic disturbances (Box 1, p41).
Edwards (1999) found that 75 per cent of female volunteers with PCOS had irregular menstrual cycles. Chronic
anovulation can result in difficult conception and increased risk of miscarriage (Aherne, 2004).
Kelley (2003) states that obesity associated with PCOS
presents primarily in the abdomen. Obesity is associated
with numerous conditions including hypertension, diabetes, dyslipidaemia and heart disease, but for women
with PCOS it produces further complications, with the
hyperoestrogenic environment converting ovarian and
adrenal androgens to oestrone peripheral fat cells (Kelley, 2003).
Management and treatment
Treatment for PCOS is complex and is limited to addressing
symptoms rather than providing a cure (Raisbeck, 1999).
It should be based on the patient’s wishes and concerns
regarding symptom management (Marantides, 1997).
Hill (2003) says the goals of treatment include suppression of hyperandrogenism to improve acne and
hirsutism, resumption of reproductive function for desired fertility, endometrium protection and the reduction
of the long-term risks of type 2 diabetes and cardiovascular disease. No single therapy treats all aspects of PCOS
and some will treat one symptom but exacerbate another, and so are mutually exclusive (Hill, 2003).
There are two types of therapy for hirsutism – cosmetic
hair removal and pharmacotherapy. Cosmetic removal
includes temporary measures such as tweezing, shaving,
waxing and depilatories, while electrolysis and laser
treatment will remove hair permanently (Hill, 2003).
These treatments should not be attempted until six
months after the start of medical therapy, or there will
be regrowth of coarse hair (Campbell and Poirier, 2000).
The pharmacological treatment of hirsutism slows
growth of new hair but does not affect established hair
(Rosevear, 2002). Reduction of testosterone to normal
levels can be accomplished by ovarian suppression with
100–200mg spironolactone daily (Campbell and Poirier,
2000). This is a diuretic as well as having an antiandrogenic effect. Improvements take 6–12 months to appear
(Raisbeck, 1999). Side-effects include menstrual irregularities, which occur in 50 per cent of patients, and it is
recommended the drug is used in combination with a
combined oral contraceptive (COC) (Hill, 2003). The COC
has also been found effective in treating hirsutism by
suppressing LH secretion and therefore LH-mediated
androgen secretion by the ovary (Rosevear, 2002).
Flutamide, a proposed alternative to spironolactone,
acts by inhibiting the androgen receptor. Liver function
monitoring is essential as hepatotoxicity has been
NT 18 January 2005 Vol 101 No 3 www.nursingtimes.net
Box 2. 10-step dietary recommendations (Harris and Cheung, 2002)
1. Aim to drink 1.5 litres (2.75 pints) of fresh water each day – vital for hormonal function.
2. Consume five portions of fruit and vegetables per day. They are powerful sources of antioxidants, vitamins,
minerals and phytochemicals, which can help to lower androgen levels in the body.
3. Eat complex, low glycaemic index (GI) carbohydrates. Low-GI foods convert food into blood sugar more
slowly, promoting a weaker insulin response. Lowering blood sugar levels balances energy, reduces
carbohydrate cravings, reduces insulin and testosterone levels, and promotes weight loss.
4. High fibre diet: aim to eat 30–50 grams of fibre daily.
5. Eat two to five portions of protein per day.
6. Eat sufficient essential fatty acids (EFAs) in the form of omega-3 and omega-6 fatty acids. Calories from fat
should contribute 20 to 25 per cent of total calories in the diet.
7. Include phytonutrients in the daily diet.
8. Eat foods that reduce cholesterol, for example oats.
9. Use herbs, spices and lemon juice to flavour food instead of salt.
10. Start the day with a good breakfast, followed by mid-morning snack, lunch, mid-afternoon snack then
supper (eating correctly at each mealtime).
reported (Rosevear, 2002). Metformin, which is used in
the treatment of diabetes, is another alternative. It is
believed that reducing hyperinsulinaemia results in a
reduction in levels of ovarian androgen and testosterone
(Raisbeck, 1999), restoring menstrual cycles, ovulation
and fertility (Rosevear, 2002).
Dianette contraceptive pill for at least six months is the
usual treatment for acne. It contains medium-dose oestrogen and cyproterone acetate, which combat testost­
erone’s effects and help to prevent the sebaceous glands
from producing more oil (Harris and Carey, 2000).
Obesity is a well-known risk factor for type 2 diabetes
and 50 per cent of patients with PCOS are obese (Hill,
2003) – although women with the syndrome can also be
underweight or have a normal body weight (Aherne,
2004). The most common treatment for obesity is a programme of at least 30 minutes’ exercise five times a
week, with dietary intervention (Kelley, 2003).
According to McKittrick (2002), exercise increases insulin
sensitivity and promotes weight loss. Further benefits
include reducing blood pressure, triglyceride levels, fasting
blood glucose levels and stress, and increasing levels of
high-density lipoprotein (HDL).
Most women with PCOS are insulin resistant, so the
diet should ideally improve insulin sensitivity and promote weight loss. The patient’s lipid profile should be
considered when determining the diet’s nutritional composition (McKittrick, 2002). Harris and Cheung (2002)
believe the secret of a healthy diet for PCOS is getting
the balance right, and recommend 10 easy-to-follow
steps focusing on different aspects of the diet (Box 2).
The COC is often used to regulate menstruation. However, it is not always suitable as it exacerbates insulin
resistance, while obesity is a relative contraindication
(Hopkinson et al, 1998).
NT 18 January 2005 Vol 101 No 3 www.nursingtimes.net
Women with anovulatory infertility and oligomenorrhoea (infrequent menstruation) need ovulation induction, for which clomiphene citrate is the drug of choice
(Rosevear, 2002). However, this increases the risk of
multiple pregnancy, and it is recommended that treatment lasts no longer than six months due to the increased risk of ovarian cancer (Hopkinson et al, 1998).
Laparoscopic ovarian surgery – most commonly ovarian
diathermy and laser – has replaced ovarian wedge resection as the surgical treatment for clomiphene-resistant
women with PCOS (Balen, 2000). However, while surgery
is effective in treating ovulation and regulating menses,
the effects are short term (Hopkinson et al, 1998).
Implications for nursing practice
Due to the complex nature of PCOS and the wide range
of possible symptoms, health care professionals need an
in-depth understanding of the condition, its pathophysiology, diagnostic measures and symptom management.
Women presenting with menstrual irregularities should
be encouraged to monitor their symptoms as this will
help in the diagnosis of possible PCOS. Once diagnosis
has been confirmed, nurses need to ensure patients receive adequate written information, such as leaflets, to
clarify issues discussed on initial diagnosis.
As a diet regimen is one of the main treatments for
PCOS, a referral to a dietitian should be discussed once
diagnosis has been confirmed. A suitable exercise regimen
should also be discussed, and the importance of both
diet and exercise should be explained to the patient.
Psychological support is vital, particularly on initial diagnosis. Nurses should be aware of the various agencies
that offer further advice and support. Counselling and
follow-up should also be made available to all women
with PCOS (Lockwood, 1997). n
further information/support
www.kathies-pain.com/pcos.htm
www.womens-health.co.uk/pcos.asp
www.pcos-support.org (US)
www.netdoctor.co.uk/
womenshealth/facts/pcos.htm
www.ihr.com/infertility (Infertility
Resources for Consumers)
www.infertilitynetworkuk.com
www.pcos-vitaline.com (personal
healthy eating plans, caring support)
www.verity-pcos.org.uk
(UK self-help group)
www.m2w3.com/acne
(acne support group)
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