Physiotherapy in PCOS

Introduction
Stein & Leventhal (1935) originally described PCOS as a syndrome manifested by amenorrhea, hirsutism, & obesity associated with enlarged polycystic ovaries Also includes a range of clinical & biochemical features like acne, elevated serum levels of LH, testosterone,

androstenedione, & insulin

 Early diagnosis & intervention necessary in PCOS women bleeding, increases risk of dysfunctional uterine metabolic syndrome, type II diabetes,

cardiovascular disease, & infertility Also growing evidence shows that PCOS women are at

increased risk of obstructive sleep apnea, depression,

non-alcoholic fatty liver disease, and certain cancers.

 12-21% reproductive age women, get diagnosed due to the complaint of infertility so in years following last delivery & with continuing reproductive senescence there is a clear tendency to

forgo long-term management of symptoms

In younger women, reproductive symptoms predominate where as with age the prevalence of metabolic features increases but can also occur in overweight younger women

 With recent significant lifestyle change in many parts of

the world, most people experiencing a sedentary

existence combined with abundance of food

modern

epidemic

of

obesity

&

consequent

hyperinsulinemia a situation which in women may precipitate expression of PCOS Treatment of current symptoms, preventive advice, and management & monitoring for future complications forms important aspect of care

Definition:
PCOS being variable nature remains a syndrome with no single diagnostic criterion but its diagnosis is based

upon the combination of clinical, ultrasound, and

laboratory features Hence the exact definition of this syndrome has been much debated & the following guidelines help in defining the presence of PCOS in women:

1990 NICHD Guidelines (National Institute of Child Health & Human Development) Patient demonstrates both: 1. Clinical and/or biochemical signs of hyper- androgenism

2. Oligo- or chronic anovulation

Exclusion of other etiologies of androgen excess and

anovulatory infertility is necessary

2003 ESHRE/ASRM or Rotterdam Guidelines

(European Society for Human Reproduction & Embryology

and American Society for Reproductive Medicine)

Patient demonstrates two of three criteria:

1. Oligo- or chronic anovulation

2. Clinical and/or biochemical signs of hyperandrogenism

3. Polycystic ovaries Exclusion of other etiologies of androgen excess & anovulatory infertility is necessary.

2006 Androgen Excess Society (AES) Guidelines

Patient demonstrates both:

1. Hirsutism and/or hyperandrogenemia

2. Oligo-anovulation and/or polycystic ovaries Exclusion of other etiologies of androgen excess & anovulatory infertility is necessary.

Pathology
Ovaries get enlarged. Volume Stroma ( 10 cm3 )

Capsule thickened & pearly white in colour

Histopathological criteria: atretic follicles degenerating granulosa cells hypertrophy of inner theca cell layer

thickened ovarian tunica

Clinical features:
Genetic basis: Postulated to be oligogenic disorder,

representing

an

autosomal

dominant

kind

of

inheritance with a small number of key genes contributing in conjunction with environmental factors (chiefly nutrition), to produce the observed clinical and biochemical heterogeneity

For clinical convinence, PCOS can be categorized into

four main phenotypes:

Biochemical/ Hyperandrogenism Chronic anovulation Polycystic ovaries Prevalence Long term health risk

Frank PCOS +

Classic PCOS +

Ovulatory Mild PCOS PCOS + -

+ 4671% Known

740% Known

+ 718% Unknown

+ 716% Unknown

Clinical features include:

Oligo- anovulation: oligio ovulation = infrequent or irregular ovulation (usually cycles of 36 days or <8 cycles a year) anovulation is absence of ovulation when it would be normally expected Hyperandrogenism: characterized by excessive

production and /or secretion of androgens

Signs include hirsutism, male pattern alopecia, acne Hirsutism: Presence of excessive facial & body hair caused by excess androgen production

 Acanthosis Nigricans:
- specific skin changes occurring due to insulin resistance - skin gets thickened & pigmented (grey brown) - Commonly affected sites are nape of the neck, inner thighs, groin & axilla

Pathophysiology:
appears to be multifactorial & polygenic It can be discussed under the following sub headings: a. Hypothalamic pituitary axis abnormality b. Androgen excess /Hyperandrogenism

c. Anovulation
d. Obesity

e. Insulin resistance

a. Hypothalamic pituitary - ovarian axis abnormality

FSH

initial stimulus for follicular development promotes conversion of androgen to estrogen

LH

in luteal phase, promotes progesterone secretion in follicular phase, induces thecal androgen production stimulates oocyte maturation at midcycle

Arcuate nucleus of hypothalamus

converts neuronal signals into endocrine signals

results into pulsatile stimulation of GnRH

Slow pulsations = FSH release predominates fast pulsations = LH release predominates

 Sensitivity of the pituitary to GnRH (pulsatability) varies with circulating estradiol (E2) concentrations during the menstrual cycle

In PCOS women, decrease SHBG levels

increased free estradiol increased pulsatile stimulation of GnRH

increase LH production & rather than FSH

b. Hyperandrogenisim:
Ovaries Theca internal layer of follicle LH Adrenal glands Zona fasciculata of cortex

Aromatase enzyme
Estrogen FSH

IGFs (insulin like growth factors)

Androgen

ACTH

In PCOS women,
ovary produces excess of androgen by: 1. Stimulation of theca layer cells by high LH 2. Defective aromatization of androgen to estrogen 3. Stimulation of theca cells by insulin growth factor (IGF 1)

c. Anovulation:

Ovary FSH

Poor follicle maturation & atresia Estrogen

Faulty aromatization

Androgen

Androgenic environment

d. Insulin resistance:
Insulin also augments LH-stimulated androgen

production, via IGF-1 receptors insulin resistance is associated with suppression of the production by the liver of sex hormone binding globulin (SHBG) SHBG is a glycoprotein synthesized in the liver

which has a high binding affinity for testosterone

compared with estrogen

e. Obesity
Close association between obesity & PCOS Around 50% of the women with PCOS have BMI 30 kg/m2 & android type of weight gain Commonly this relationship is misinterpreted, supposing that PCOS status somehow leads to obesity But in fact, obesity drives polycystic ovaries to be more

clinically manifestive

 Obesity might convert some women with occult polycystic ovary (PCO) morphology to clinically obvious PCOS Therefore obese women are over-represented in clinics

while relatively asymptomatic lean women remain at

home Obesity can affect ovulation & pregnancy rate which can lead to infertility

 Some of the factors contributing to obesity are genetic

make up, BMR & physical activity

Genetic make up:

3040% of obesity genetically determined

Also couples tend to match w.r.t lifestyle preferences i.e. obese women tend to have obese partners so many genetic factors get pooled passed on to their offspring

BMR:

BMR is not influenced by PCOS status

It falls sharply at the age of 18 to 20 yrs when vertical

growth abruptly stops & is translated in many into

expansion of girth Hence late adolescence is a common problem age for women with PCOS Physical activity:

Current obesity epidemic is related to diminished activity

due to sedentary lifestyle

Assessment
Subjective assessment: Chief Complaints: Oligo - Amenorrhea Infertility Obesity Hirsutism / Male pattern alopecia Obstetric History: Gravida & Parity

Past medical History:

Last normal menstrual period (LNMP)

Oligo /amennorhea

Infertility
Gestational diabetes / Diabetes Mellitus Blood Pressure Hyperlipidemia

Personal History:

Diet, Sleep
Smoking / Alcohol

Exercise
Objective assessment:

BMI using following criteria:

BMI <18.5kg/m = underweight BMI 18.5-24.9kg/m = lean BMI 25.0-29.9kg/m = overweight

BMI 30.0-34.9kg/m = obese

BMI 35kg/m = morbidly obese Waist circumference Waist circumference >80cm = risk of metabolic complications

Waist circumference >88cm = substantially risk of

metabolic complications Skin examination: Acanthosis Nigricans Male pattern alopecia /Hirsutism /Acne

Investigations:
Ultrasound : Abdominal or Trans-vaginal Multiple (12) follicular cysts measuring about 2 9 mm in diameter are found crowded around the cortex like strings of pearls Bright echogenic stroma

Complete lipid profile:

Total cholesterol = should be <4 mmol/L

LDL-C levels should be <3.4 mmol/L

(without CVD risk factors)

LDL-C levels should be <1.82.6 mmol/L

(with metabolic syndrome or type 2 diabetes )

HDL-C levels should be >1.0 mmol/L Triglycerides- levels should be <1.7 mmol/L

Hormones & Normal ranges

Testosterone levels (T) 0.53.5 nmol/l SHBG levels 16119 nmol/l LH levels 210 IU/l FSH levels 28 IU/l Prolactin < 500 mU/l TSH 0.55 IU/l

Management
Non Pharmacological: (Lifestyle management)
Includes exercises, diet & behaviour modification

Fact that close association exists between obesity &

PCOS has resulted into increased research Large no. of small, uncontrolled trials showed weight loss upto even 5% through lifestyle management offered considerable benefits

 Like decrease in abdominal fat, hyperandrogenism & IR

Also it improved lipid profile, ovulation, menstrual

cyclicity, & fertility, risk factors for DM type 2 & psychological health in overweight women with PCOS Helpful in targeting weight loss & prevention of weight gain Hence considered as first-line treatment for a large proportion of women with PCOS

Exercises
Exercise alone is a significant determinant of BMR Cardiovascular exercise expenditure short-term energy

increases in BMR,

thus improves overall daily energy expenditure Exercise therefore must be at the forefront of management of obese women with PCOS

Systematic review from Human Reproduction Update, 2010 Intensity Moderate

60 70 % VO2 max, 75 80 % HR max

Duration 3 times/ week for 12 weeks 90 min /week Type Aerobic

Evidence-based Australian guidelines for the assessment and

management of PCOS, 2011

Intensity Moderate to high

(60% - 90% of HR max) for 90 min /week

Duration Total of 150 min /week Especially for those with BMI 25kg/m2 (overweight/obese) Type Aerobics (Circuit training, Speed walking, Brisk walking, Medium paced swimming or cycling)

Exercise-Induced Weight Reduction and Fertility Outcomes in

obese and infertile PCOS women Intensity Duration 60% to 85% of HR max, 13 15 RPE Starting from 15 min initially to 45 min continuously (including warm up & cool down) Frequency 3-5 times /week Type Aerobic activity (walking, jogging)

RCT on Effects of Exercise on Lipoprotein Particles in women

with PCOS Frequency ~228 min /week Duration Intensity 4060% of VO2 max 1624 weeks total (812-wk ramp-up followed by 12-wk moderateintensity exercise program) Type Aerobic exercise

Symposium on Effects of lifestyle modification in PCOS Frequency 35 days /week Intensity Low to moderate (gradually increase)

Duration
Type

3060 min (including warm up & cool down)

Low-impact activities (e.g. walking, cycling, low-

impact aerobics )
Resistance training (23 times /week)

Diet:

Reduced-energy diets:
(5001000 kcal/day reduction)

reduces body weight by 710%

over a period of 612 months A low carbohydrate diet is generally prescribed Mainly consists of saturated fat, with increased consumption of fibre, whole-grain breads & cereals, and fruit & vegetables

Behavioural therapy: Psychological factors likely to affect women with PCOS are: - depression and/or anxiety - psychosexual dysfunction - eating disorders - negative body image - health related quality of life these factors are mainly considered and managed to optimise engagement & adherence

Pharmacological:
Metformin: Anti-diabetic drug shown to prevent the cardiovascular complications of diabetes Helps to reduce LDL, cholesterol and triglyceride levels, and is not associated with weight gain. Metformin improves insulin resistance, improves

aromatisation of androgens

Gonadotrophins: Clomifine citrate: selective estrogen receptor modulator (SERM) Normalizes the hypothalamic pitutary - ovarian axis

Helps in maturation of the follicle & thus in ovulation

Often results in the development of multiple mature

follicles with a potential risk of multiple pregnancies

Cosmetic Therapy Mainly considered in patients with signs of hyperandrogenism Drug therapies generally take 6 to 9 months or longer to

show any improvement of hirsutism

So physical treatments like electrolysis, waxing and

bleaching may be helpful while waiting for the medical

treatments to work

Surgical a. Laparoscopic ovarian drilling: A puncture of 410 small follicles with electro-cautery, laser, or biopsy needles is done. After the surgery, there is restoration of ovarian activity so the serum concentrations of LH & testosterone also

falls

 A fall in serum LH concentrations both increases the chance of conception and reduces the risk of miscarriage Bariatric surgery

Considered in morbidly obese women BMI 35kg/m2

Summary

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Thank You