Overview normal physiological development; skeletal growth, maturation of the reproductive tract, development secondary sexual characteristics, CNS maturation, personality and psychology of the female adolescent.

1. Paediatric & Adolescent Gynaecology
Michelle M Fynes
MD MB BCh (Hons) BAO (Hons) MRCOG DU(RANZCOG) DipUS
Subspecialty Accredited Urogynaecologist RCOG RANZCOG
Specialist Complex Peri-partum Childbirth Injury
Adolescent and Paediatric Gynaecology
Consultant Urogynaecologist & Honorary Senior Lecturer
Invited Speaker presenting to: Masters/Diploma Women’s Reproductive Health,
University College Hospital London, Chenie Mews London UK, 7th May 2018

2. Institute of Medicine
Quality care –
– Safe
– Effective
– Patient centred
– Timely
– Efficient
– Equitable
Adverse event/SUI/ Critical Incident reporting
Audit (measurement process and outcome)
CPD
Mandatory training/updates

3. Medical Ethics- Four Key Principles
• Beneficence – Provision of benefit whilst balancing this against risk. Also for individual
situation/procedure/treatment taking into account overall needs of the individual.
• Non-maleficence – ‘Primum non nocere’ - First of all do no harm. Do not attempt treatment
where there will be no benefit and likely risk of harm.
• Justice – Implies a duty to spread benefits and risks equally in a society. Treatment should be
available to all who may benefit from it. There should be no discrimination on the grounds of
factors such as age, disability or lifespan.
• Autonomy - Patients making their own informed decisions rather than healthcare (parents?)
providers making decisions for them. Autonomy requires that a person with capacity is
adequately informed, free from undue pressure and that there
is consistency in their preferences
Adolescent Gynaecology
Age of consent?
Capacity?
Rights of the parents?
‘It is incumbent on all health professionals to act within the law’

4. Adolescent Gynaecology
Objectives
• Overview normal physiological development; skeletal growth, maturation of
the reproductive tract, development secondary sexual characteristics, CNS
maturation, personality and psychology of the female adolescent.
• Adolescents presenting with Specific Gynaecology issues:
– Menarche and physiological changes
– Congenital disorders
– Adolescent gynaecological disorders
• Problems unique to adolescents,
• General gynaecological disorders presenting in adolescents
• Adolescent urogynaecology
• Haematological disorders presenting with secondary gynaecological symptoms
• Dermatological conditions presenting with gynaecological symptoms
• Sex and the adolescent - STD’s, PID, cervical screening, HPV vaccination
• Teenage Contraception and Pregnancy
• Adolescent gynaecology and psychiatry - Body dysmorphic disorders
• Forensic and legal aspects to adolescent gynaecology

5. Female Development
• Embryology – Chromosomal and congenital fetal
development disorders
• Childhood and pre-menarche
– Normal adolescent development
– Skeletal growth
– BMI
– Maturation of the reproductive tract
– Development of the secondary sexual characteristics
• Adolescent Neuro-psychology
– CNS development and maturation
– Adolescent female personality
– Sexuality and sexual identity

6. XX Embryology
• In females the genital organs
comprise of gonads, reproductive
ducts and external genitalia.
• Gonadal differentiation occurs
before the end of the embryonic
period.
• Both the reproductive ducts and
external genitalia differentiate
before the end of the first
trimester.
• Development of the female genital
tract continues in utero. The
gonads descend in utero in XX.
• Maturation of the genital tract is
continuous during childhood
through to puberty.
In-utero development female gynaecological tract
Phase of genital development Gestational age
weeks
Indifferent gonadal phase 4–6
Gonadal differentiation 7
Ductal differentiation 9–11
External genitalia
differentiation
10–12

7. Development of the
Ovaries from Indifferent
(undifferentiated) Gonads:
a) Gonads develop from primitive germ cells
precursors oocytes), mesothelium posterior
abdominal wall and adjacent mesenchyme.
The indifferent gonads have a cortex (ovarian
parenchyma) and medulla (ovarian stroma).
Initially they appear as primitive longitudinal
streaks in intermediate mesoderm adjacent to
the mesonephros.
b) Magnified undifferentiated gonad during 5–6
weeks. The primordial follicles develop in the
yolk sac migrating to the gonadal ridge
sustained by the primary sex cords.
c) Primary cords are transitory regressing by 8
weeks. Cortical (secondary cords) maintain
ovarian follicular development. Ovaries are
identifiable by 10 weeks.
d) The genotype and chromosomal sex is set at
conception. The fetus has bipotential sex
development until week 12. Phenotype
depends on sex chromosome, hormones,
biochemistry.
e) An immature female will develop in an XY if
problem with any of 3 factors – SRY protein (Y
chromosome)-testicular differentiation and
production androgens and AMH (prevents
female genital duct differentiation).
f) Further maturation immature female
dependent on oestrogens (disorders of sex
development)

8. Pelvic Descent of the Ovary
1. Fetal abdominal ovary descends into the
pelvis lying in close approximation to the
fimbrial portion of the lateral aspect of the
paramesonephric duct (future fallopian tube).
2. Maldescent of the ovary occurs when the
ovary lies above the pelvic brim.
3. Rarely the ovary may be located in the
inguinal canal or more inferiorly at the labium
majorum (right hand side of pelvis).
4. The canal of Nuck is a potential space which
results from a patent evagination of the
peritoneum to the labium majorum
5. Ovarian maldescent is rare, may occur from
paraspinal posterior abdomen to pelvic brim.
Results from short mesovarium and
infundibulopelvic ligament with elongation of
utero-ovarian ligament
6. Ovary contains 2-4 million follicles at birth
and 400,000 at menarche.

9. Relationship of Fetal Genital and Urinary Systems
Three stages of renal development -
a) The pronephros and mesonephros, are
transitory structures critical for
development of metanephros
(permanent kidney). Paired pronephros
develops in the cervical region week 3
and regress week 5
b) Mesonephros forms below pronephros
in the thoracic region week 4 (interim
kidneys). Paired mesonephric ducts
(Wolffian duct) drain the mesonephros
into the cloaca ventral to the laterally
placed nephrogenic cords (b)
c) XX fetus mesonephros and mesonephric
ducts involute by week 12
d) Vestigial structures such as the
Gartner’s duct, epoophoron and the
paraoophoron may persist Embryonic genitourinary tract at a) 4 weeks and b) 6–8 weeks

10. Development Upper Genital Tract - Fallopian Tubes, Uterus, Cervix, upper Vagina
Paramesonephric (Müllerian) ducts arise from mesoderm lateral
to the mesonephric ducts (week 7). They grow caudally, coursing
lateral to the urogenital ridges (week 8 ). They fuse (Müllerian
organogenesis) - initial development upper two-thirds of vagina,
cervix, uterus and fallopian tubes
The cranial end of the fused ducts the future uterus contains
mesoderm that forms uterine endometrium and myometrium.
Unfused cranial ends of the paramesonephric ducts (funnel
shaped) remain open as the fimbriale of the fallopian tubes.
Caudal end of fused ducts forms upper two-thirds of the vagina.
Lateral fusion of the paramesonephric ducts (week 7-9) when
lower parts paramesonephric ducts fuse. At this stage midline
septum is in the uterine cavity regresses week 20 (uterine septal
defects).
Vertical fusion (week 8) when the lower most fused
paramesonephric ducts fuse with the ascending endoderm of the
sinovaginal bulb. Lower third of the vagina is formed as the
sinovaginal node (bulb) canalises.

11. Meso-nephric Vestigial Remnants
Embryological Vestigial XX Structures
In the XX fetus mesonephric & paramesonephric
ducts co-exist. Mesonephric (Wollfian) ducts
regress. Vestigial remnants may cause pathology.
1. Gartner’s Duct
Gartner’s ducts are paired remnants of the
mesonephric duct . May give rise to Gartner’s
duct cysts normally in the broad ligament (BL).
2. Canal of Nuck (XY processus vaginalis)
Virtual space. If remains patent it may form a
peritoneal pouch (cyst) in the labia majorum.
3. Epoophoron ( XY epidydimis)
Most cranial part of the mesonephric duct
remnant in the lateral broad ligament. May
communicate with Gartner’s ducts (inferior BL)
4. Paraoophoron (XY paradydimis)
Mesonephric remnant located in the medial BL

12. Development of the Lower Genito-urinary Tract and
Differentiation of the Cloaca
a) The cloaca – the cloacal membrane
(CM) forms week 3 it is imperforate
at this time.
b) Descent uro-rectal septum week 4-6
fusion week 7 to the inner CM.
Partition cloaca into urogenital and
anorectal compartments (anal
membrane). UG membrane
perforates free communication
between primary UG sinus and
amniotic cavity. Folds around the UG
membrane (urethral folds) and
around the anus (anal folds).
c) Formation genital tubercle and
urogenital sinus (UGS). The phallic
(*) and cranial () portions of the
pelvic UGS form the vaginal
vestibule and female urethra,
respectively.
d) Canalisation of the vagina at the
vaginal plate onto the UGS (vertical
fusion).
e) Definitive vaginal vestibule

13. Development of the External Genitalia (EG)
Week 4 - Genital tubercle results from mesenchymal proliferation and a protophallus
ventral to the cloacal membrane begins to develop.
Week 6- Urethral groove and anal pit form causing focal depressions on cloacal
Membrane (a). Primary urethral (urogenital) folds surround primary urethral groove.
Genital/labioscrotal swellings form lateral to the folds.
Week 7 - Cloacal membrane involutes and primary urethral groove becomes
continuous with the now definitive urogenital sinus.
Week 8 - Secondary urethral groove forms with deepening/widening of the primary
urethral groove
Week 10 – EG display sexual differentiation (c). Unfused parts of labioscrotal (genital)
swellings give rise to labia majora, fusing anteriorly to give mons pubis, anterior labial
commissure, and behind the posterior labial commissure. Urethral folds fuse behind
forming frenulum of the labia minora. Unfused urethral (urogenital) folds form labia
minora. Unfused genital swellings enable the urogenital sinus to open into the anterior
(urethral) part of the vagina and the vaginal vestibule.
Week 14 - Genital tubercle becomes recognisable as the clitoris (d)
Fetal development stages (weeks) EG a) 4 (indifferent),
b) 6–7, C) 9–11, d) 12 (full differentiation)
Week 7 until now EG are sexually undifferentiated
Week 10 sexual characteristics appear
Week 12 complete differentiation EG

14. Development Female Genital Accessory Glands
The accessory urethral glands include-
1. Lesser vestibular or paraurethral
glands (Skene) and urethral glands:
Arise from the urogenital sinus from
endodermal (epithelial) buds growing into
the urethral mesenchyme.
Pathology: Skene’s cyst, abcess, urethral
diverticulum, recurrent urethritis, urethral
syndrome, dyspareunia, discharge.
2. Greater vestibular (Bartholin’s) glands:
Paired glands forming week 12. Emptying
into the vaginal vestibule at 4 and 7 oClock
Pathology: Bartholin’s cyst, abscess
.

15. Congenital anomalies
Gartner duct cyst MRI–Absent
uterus. (A)axial (B) coronal. GDC
(arrow) anterior/lateral vagina
(arrowhead). B, bladder.
Imperforate hymen XX years – US
distended vagina (V) fluid level extends
well below level of the bladder neck
(B)(arrow). (B) MRI same as US.
Arcuate uterus – XX 15 years 3D US
image. Normal variant incomplete
resorption uterovaginal septum.
MURCS Association -
XX 3-month-old infant
imperforate anus,
congenital heart disease
a single left kidney. (A)
(B) Sagittal/ coronal MRI
uterus rudimentary
unicornuate (arrow).
vagina (asterisks) , the
bladder (B) and rectum
(R). The sacrum appears
dysplastic. (C) A single left
kidney is identified (K).
There is duplication of
the IVC (arrows). Small
syrinx is present
(arrowhead).
MURCS Association-
Klippel-Feil deformity.
conductive deafness .
Absent vagina (MRKH
syndrome type 2).
Mullerian & renal aplasia.
Cervico -horacic somite
dysplasia. Prevalence: 1-5
/ 10 000. Inheritance:
Sporadic autosomal
dominant.

16. Personality and Psychology of the Female Adolescent.
Sex differences in the course of personality
development: A meta-analysis. Cohn, Lawrence D.
Psychological Bulletin, Vol 109(2), Mar 1991, 252-266.
Size and stability of sex differences in personality growth change
through adolescence and adulthood. Studies using the Washington
University Sentence Completion Test of ego development served
as the primary source data (65 studies more than 9,000 students)
Sex differences in ego development moderately large among junior
and senior high-school students (female advantage), declined
significantly college-age adults, disappeared among older men and
women. Sex differences were stable during early and middle
adolescence. The greater maturity displayed by adolescent girls is
not an artefact of superior verbal abilities (evident at 11 years).
Sex differences in ego development were more than twice the
magnitude of differences in vocabulary skills (JS Hyde, MC Linn).
Reviews of sex differences in moral judgment, aggression, and
empathy, suggest that adolescent girls achieve developmental
milestones earlier than boys, a difference that declines with age.
Anthony Reyniers and His Family (1631) by Cornelius de Vos
Philadelphia Museum of Art.
Development in Adolescence and
Emerging Adulthood
A. Physical
B. Cognitive
C. Psychosocial

17. Erikson’s Stages of Psychosocial Development

18. Menarche and Physiological Changes
Puberty
At birth, females have a predetermined number
primordial follicles arrested during meiosis 1 at the
diplotene stage of prophase until stimulation at
puberty. Hypothalamus is in a quiescent state.
At approximately 8 years, GnRH is synthesized in the
hypothalamus and released.
The adrenal cortex begins to produce DHEA initiating
adrenarche (ie, the development of sexual hair).
Progression of puberty begins with breast budding
(thelarche), accelerated growth, and menses
(menarche).
Pubarche, which is independent from GnRH function,
typically occurs between breast budding and
accelerated growth but may occur anywhere along the
puberty timeline.
USA average age at menarche is 12.6 years, (R 9-15
years). 16 years is 3 SD’s above
Menarche and sustained menstrual cycles requires
normal function of the endocrine HPO axis any
disruption in this axis may result in
amenorrhea/oligomennorhoea.
Defining the level of primary dysfunction is critical in
determining the pathophysiology of amenorrhea.
Tanner stages 1-5
Stage I (Preadolescent) - Only papilla elevated above level of the chest wall.
Stage II - (Breast Budding) - Elevate breasts/ papillae (small mounds), wider areola
Stage III – breasts/areolae continue enlarging no separation of contour.
Stage IV – areola/papilla elevated, secondary mounds, increase overall breast tissue.
Stage V – Mature breasts, papillae extend above breast contour, areolar recession.
Stage I - Vellos hair over pubes, no more than on abdominal wall. No sexual hair.
Stage II - Sparse, long, pigmented, downy, straight/slightly curled, hair along labia.
Stage III - Darker, coarse, curlier hair now spread sparse over junction of the pubes.
Stage IV – Adult hair distribution , reduced total quantity, no hair on medial thighs.
Stage V - Hair adult quantity/type, appears as inverse triangle (feminine type).
Spread to medial surface thighs but not above the base of the inverse triangle
Puberty Before Age 10: A New ‘Normal’?
30th March 2012

19. Precocious puberty: a comprehensive review of literature.
Cesario SK, Hughes LA. J Obstet Gynecol Neonatal Nurs. 2007;36(3):263-74
Incidence – 1 in 7 Caucasian , 1 in 2 African American girls start to develop breasts or pubic
hair by age of 8 years. Precocious puberty affects 1 in 5,000 . 10 times more common in girls.
Factors influence early sexual maturation female children are multi-factorial-
• Genetic, Ethnic, Paediatric obesity, Environmental toxins disrupt endocrine function
(chemicals, toxins, plasticizers, infant feeding, skin/hair products, ART)
• Psychosocial stress, and early exposure to a sexualized society
Precocious Puberty: How Early
Is Early?
Precocious puberty: The diagnosis depends on the
definition. Published on October 31, 2009
by Jean Mercer, Ph.D.
Although there are clear social and psychological
concerns about precocious puberty, the most
serious reason for paying attention to early
development is the possibility that this growth is
driven by abnormalities in the child's central
nervous system.
However, Kaplowitz, the author mentioned earlier,
referred to a French study in which girls under 6
who showed signs of precocious puberty were
compared to girls between 6 and 8. About 6% of
the younger children did have some central nervous
system problem, but only 2% of those over 6 had.
This suggests that girls showing precocious puberty
between 6 and 8 years of age probably do not need
further evaluation for nervous system problems.
Precocious puberty in boys, defined as
development before age 9, is quite rare (1 in
10,000 in the United States), but when it does occur
is much more often associated with central nervous
system problems that need treatment.
Update on precocious puberty: girls are showing signs of puberty earlier, but most do not
require treatment. Kaplowitz P. Adv Pediatr. 2011;58(1):243-58
Puberty was considered precocious in girls < 8 years; recent studies indicate that signs of
early puberty (breasts and pubic hair) are often present in girls (particularly black girls) aged
6-8 years. Early onset of puberty can cause several problems. The early growth spurt initially
can cause tall stature, but rapid bone maturation can cause linear growth to cease too early
and can result in short adult stature.
Premature pubarche and premature thelarche are 2 common, benign, normal variant
conditions , resemble precocious puberty but non/slow progressive . Premature thelarche
isolated appearance breasts, usually in girls <3; premature pubarche pubic hair without other
signs of puberty in girls/boys <7-8 years. History, examination, growth curve help distinguish
normal variants from true sustained precocity. Must differentiate central precocious puberty
(CPP) from precocious pseudopuberty (PSP). CPP is gonadotropin-dependent, early
maturation of the entire HPG axis, full spectrum physical/hormonal changes puberty. PSP
less common, refers to conditions where increased production sex steroids is gonadotropin-
independent . Correct diagnosis aetiology sexual precocity critical, evaluation/treatment
precocious pseudopuberty is different than that for central precocious puberty
Precocious Puberty ?

20. Paediatric and Adolescent Gynaecological (PAG) Service
A study of paediatric and adolescent gynaecology services in a
British district general hospital. S McGreal, PL Wood. BJOG 2010;
117(13):1643–1650
PAG service Kettering General Hospital established 1993 Analysis referrals:
800 cases over 15 years (1999-2004)
Recurrent vulvovaginitis (relapsing/chronic) 18%
Labial adhesions 14%
Dysmenorrhoea/menorrhagia 13%
Suspected precocious puberty 6%
Genital tract abnormality (18 cases) 0.02%
Primary amenorrhoea (17 cases) 0.02%
Secondary amenorrhoea
Suspected sexual and or physical abuse 3%
Incontinence or urinary symptoms 5%
Lower abdominal pain 7%
Lichen sclerosus 3%

21. Embryo 4 layers – Lower Genito-Urinary Tract
1 (pink ) phalloclitoris- head of penis or clitoris
2 (orange) phallic shaft or clitoral body and labia minora.
3 (green) inset membrane widen/close fetus develops
forms urethra, and if XX the vagina.
4 (blue) labioscrotal swellings, labia majora or scrotum.
Typical XX and XY - 4 sectors embryonic
genitalia (EMG) differentiate to typical XX
or XY . Pink phalloclitoral head points
downward in typical XX upright in typical
XY. Orange body of the phalloclitoris is
buried beneath labia in XX closes around
urethra forms penile shaft XY. Many forms
sex variance. Not random. Intersex
conditions produced by regular patterns
development variance (1-4) parts EMG.
Clitoromegaly /XX
pseudohermaphrodite (CAH) - Early
accurate diagnosis, counsel parents on
therapeutic options. Paradigm early
gender assignment challenged by
clinical/basic science research, shows
gender identity begins in-utero.
Surgical genital reconstruction
successful but psychological/social
implications shifted paradigm from
early reconstruction.
Disorders Sexual Development
(DSD)-Intersex Conditions
Revised Nomenclature of Disorders of Sexual Development
Previous Revised
XX pseudohermaphrodite 46,XX DSD
XY pseudohermaphrodite 46,XY DSD
True hermaphrodite Ovo-testicular DSD
XX male 46,XX testicular DSD
XY sex reversal 46,XY complete gonadal dysgenesis
Sex chromosome DSD
45,X (Turner syndrome and variants)
47,XXY (Klinefelter syndrome and variants)
45,X/46,XY (mixed gonadal dysgenesis, ovotesticular DSD)
46,XX/46,XY (chimeric, ovotesticular DSD)
46,XY DSD – Disorders of-
Testicular development (complete/ partial gonadal dysgenesis)
Androgen synthesis (complete and partial androgen insensitivity
AMH/receptor, androgen biosynthesis defect
Other (severe hypospadias, cloacal exstrophy)
46,XX DSD – Disorders of-
Ovarian- (ovotesticular DSD, testicular DSD, gonadal dysgenesis)
Androgen excess (fetal CAH, fetoplacental, maternal)
Other (vaginal atresia, cloacal exstrophy)

22. DSD- Pseudo and True Hermaphrodites
CAH
Definition - CAH masculinized external genitalia, excess adrenal androgen -in utero, or late
onsetin adolescence. Most e block in production cortisol . Enzyme defect 21-hydroxylase
(P450c21). Deficiency this enzyme 95% cases CAH.
Most severe form blocks aldosterone & cortisol- salt-wasting , shock , significant virilization.
Various mutations CYP21B gene responsible for 21-hydroxylase deficiency. Severity CAH
determined by specific gene mutation.
Onset - excess androgens occurs 60-80-mm stages fetus. Build-up of excess precursors
progesterone and 17-hydroxyprogesterone as unable to convert to aldosterone & cortisol.
Shunted to production androstenedione & testosterone. Excess androgens masculinize EG
in female. Degree masculinization depends on time onset CAH – clitoromegaly, psuedopenis.
The gonads are undescended ovaries. The disturbance of metabolic processes requires
prompt diagnosis and treatment.
CAH 5–8% due 11ß-hydroxylase deficiency, 11-deoxycortisol not converted to cortisol and
virilization will occur due to shunting of precursors into androgen biosynthesis, similar to
21-hydroxylase CAH. 11-deoxycorticosterone not converted corticosterone and
aldosterone, to a degree with this block .
3ß-hydroxysteroid dehydrogenase deficiency leads to decreased synthesis of
glucocorticoids, mineralcorticoids, androgens, and estrogens. These neonates severely ill
and this enzyme deficiency is fatal. Females may be slightly virilized and males may be
incompletely masculinized. Mild, late-onset present with hyperandrogenemia (recently
described). Prenatal treatment - At 4–5 weeks gestation- dexamethasone reduces degree
virilization in fetus. XX -excess androgen untreated (pseudohermaphrodites)
True hermaphrodites possess both testicular and ovarian tissue. Both types may be
contained in one gonad, ovotestes, or one side may be an ovary other side testis. Internal
structures correlate to adjacent gonad. EG are ambiguous, may be sufficiently developed to
do XY gender assignment. 75% develop gynecomastia , > 50% menstruate puberty, perhaps
making female sex assignment easier.
Adrenal steroidogenesis

23. Ovarian anomalies – Turners syndrome
• Genotype (sex) is determined at conception.
• Phenotype (morphologic) sex differentiation
shown in the ovaries week 7.
• Primordial germ cells found 24th day near
allantois. Germ cells proliferate, migrate to the
genital ridge, by week 5, become elevated and
thickened.
• Sex differentiation visible early week 8.
• Proliferation oogonia (germ cells) by mitosis
continues until 15th week at 16 weeks primary
follicles seen.
• Ovary is a discrete organ, “descends” to pelvic
brim and rotates laterally.
• Ovarian anomalies rare other than streak ovaries
(gonadal dysgenesis). Complete absence ovary is
extremely rare usually associated renal agenesis
absence ipsilateral fallopian tube.
• Gonadal dysgenesis usually streaks of CT tissue
called "streak gonads“. Dysgenetic ovaries
absence of follicular structures and oocytes. Most
common cause is Turner syndrome, 45X.
• Phenotypic females with streak gonads can also
have XX gonadal dysgenesis, XY gonadal
dysgenesis or mixed gonadal dysgenesis.

24. PAG - Suspected Precocious Puberty
PAG Clinic – Precocious puberty
• 44/800 (6% referrals over 15 years) with
suspected or proven precocious puberty.
• Mean age 6years (R11 months-10 years).
• Majority present with axillary or pubic hair.
• 20% of those with suspected precocious
puberty were confirmed, treated LHRH
analogue: (youngest 6 years)
• 27% isolated adrenache
• 53% remaining appropriate puberty for age.
• 39% remained under active monitoring and
27% discharged, reassurance/puberty pack.
• 5% vaginoscopy for vaginal bleeding
• 9% were referred to other centres for
genetic, endocrinology, neurosurgical
opinions, MDT approach.
A study of paediatric and adolescent gynaecology
services in a British district general hospital
S McGreal, PL Wood. BJOG 2010; 117(13):1643–1650

25. Menstrual Dysfunction
Primary amenorrhea - no menses by 16 years, normal growth,
secondary sex characteristics. By 13 years not menstruated, onset
puberty, no breast development, workup primary amenorrhea.
Secondary amenorrhea - cessation sometime after menarche
Oligomenorrhea - menses occurring at intervals > than 35 days

26. PAG – Primary & Secondary Amenorrhoea
Primary amenorrhoea
Peak age 16 years (R14-25 years)
18% discharged with no action needed
18% actively monitored over period of time.
Treatment
41% COCP
18% HRT
12% multiple therapies
5% advice from a dietician
Outcomes
76% constitutional/spontaneous menses
6% Turners syndrome
6% Primary ovarian failure
6% Prader–Willi syndrome
6% Weight-related amenorrhoea
Secondary amenorrhoea
Peak age 16 years (R12-18 years).
Pathology:
24% discharged at the first appointment/no further action
6% primary ovarian failure
6% secondary regular medications (Na valproate, depot provera)
3% pituitary microadenoma
3% hypogonadotrophic amenorrhoea
3% weight-related amenorrhoea
Treatment
40% COCP
9% HRT
3% Bromocryptine
Outcome:
6% were actively monitored
15% review by a dietician
79% spontaneous return of menstruation without further tests
A study of paediatric and adolescent gynaecology services in a British district
general hospital. S McGreal, PL Wood. BJOG 2010; 117(13):1643–1650

27. PAG Service – Menstrual Dysfunction
Referral pattern:
13% Dysmenorrhoea and/or menorrhagia.
17% had been treated by the GP.
3% presented as an emergency admission
Median age: 14 years
Symptoms:
33% menorrhagia
25% dysmenorrhoea
17% dysmenorrhoea and menorrhagia
8% prolonged periods
6% frequent periods.
Treatment
34% COCP
14% tranexamic acid
14% depot provera
10% advice and education
8% mefenamic acid
5% iron supplements
2% HRT
1% Mirena IUS
46% combination of therapies
5% laparoscopy +/-treatment for endometriosis.
A study of paediatric and adolescent gynaecology services in a British district general hospital
S McGreal, PL Wood. BJOG 2010; 117(13):1643–1650
Background
25% of adolescents have marked menstrual disturbance
Most of these cases are dealt with by GP
More difficult cases are referred to the PAG service along
with difficult contraception issues, especially in adolescents
with developmental delay.
Concomitant haematological disorders multidisciplinary
approach

28. Haematological Disorders –
Presenting with Gynaecological Symptoms
Haematological disorders
- von Willebrand disease;
- acquired haemophilia;
- carriers of haemophilia;
- Factor XI deficiency
Mennorrhagia
• Excessive haemorrhage is one of the commonest symptom when adolescents present to a gynaecologist.
• Less commonly, the bleeding is due to an undiagnosed underlying coagulation defect, the commonest of which is von
Willebrand (vWD) disease.
• Menorrhagia is a common, and may be the only, clinical manifestation of an inherited bleeding disorder. Screening 150
young women with menorrhagia, vWD was diagnosed in 13% and other hereditary haemorrhagic disorders in another 4%.
• Menorrhagia with onset at the menarche was predictive of an inherited bleeding disorder in 65% of vWD and 67% of FXI
deficiency. Testing for bleeding disorders should be considered in girls with early onset menorrhagia.
• Increased awareness among gynaecologists of these less common causes and close collaboration with the local
haemophilia centre and availability of management guidelines are essential for optimal outcome
Kadir, Aledort. Clinical & Laboratory Haematology 2000;22(s1):12-16
Known haematological disorders
• 116 women - 66 vWD, 30 carriers haemophilia, 20 factor XI (FXI) deficiency. Interview and gynaecological history obtained.
Menstrual loss objectively assessed by pictorial blood assessment chart (PBAC). Comparison with age-matched control
group (69 women). Menorrhagia (PBAC score> 100) confirmed in 74%, 57% and 59% of women with vWD, carriers of
haemophilia and FXI deficiency, respectively, in comparison with 29% of controls (P = 0.001). PBAC scores were higher in
vWD patients with a von Willebrand factor activity (vWF:Ac) of ≤ 30 IU dL−1 compared to those with higher levels.
• No relation between PBAC score and the severity of the disease in FXI deficient and carriers of haemophilia.
• Duration of menstruation significantly longer (P = 0.001), episodes of flooding significantly more common (P = 0.001) in
patients with inherited bleeding disorders compared to controls.
Kadir, Ecconomides, Sabin, Pollard, Lee. Haemophillia 1999;5(1):40–48.

29. Hirsutism -
Affects 5-15% XX
Ferriman Gallwey Score –
Clin assessment of body hair growth in
women. Clin Endocrinol Metab.
1961;21:1440-1447.
Causes -
1. PCOS (70–80% hirsutism cases)
2. Endocrine: Hypothyroid , acromegaly, hyperprolactinemia,
cushings -cause hyper androgenism
3. Androgen tumours ovary (arrhenoblastomas; Leydig, hilar ,
thecal )/ adrenal ( 1in 300-1000) hirsutes/50% malignant)
4. Drugs – indep androgens, phenytoin, minoxidil, diazoxide,
streptomycin,high-dose steroids, psoralen, penicillamine.
5. Non-classic CAH (AR) -1.5–2.5% cases, 21-hydroxylase
deficient, >17-hydroxyprogesterone (androgenic)
6. Idiopathic (hyperandrogenism/hirsutism )6-7%
Management - (9–12 months for maximum effect)
Lanugo- soft hair covers fetus shed by 4 months old
Vellus - soft, >lanugo (2 cm), non-pigmented covers body
Terminal hair-long pigment, eyebrows, scalp, axilla, pubis
3 phases hair growth-
Anagen- active growing; Catagen- involuting, stops growing;
Telogen- resting phase, hair is shed.
Testosterone converted follicle by 5-reductase to potent
dihydrotestosterone (DHT). Weaker- androstenedione , DHEA
metabolised skin to testosterone , DHT - induce s hair growth.
Mild (FG score 8–15)- Treat cosmetic
Moderate–Severe (FG 15) - androgen excess investigate causes
Free testosterone level most sensitive . Levels > 1.5–2 ng/ml
suggest neoplasm – If DHEA (adrenal) as not produced ovary.
Non-classic CAH- testosterone , 17-hydroxy progesterone (17-
OHP), elevated early morning. PCOS – (17-OHP)slightly elevated
Levels >200 ng/dl suggest CAH. USS look for PCO change.
Treat- OCP (Dianette), cyproterone acetate, cosmetic- laser,
electrolysis, bleaching, waxing, shaving), topical facial
eflornithine (Vaniqa®). Off license use -spironolactone,
antiandrogens, such as flutamide, finasteride high-dose
cyproterone acetate.

30. PCOS
PCOS- 5-10% XX reproductive age
• Oligo or amenorrhoea
• Infertility and Miscarriage
• Acne
• Hirsutism, alopecia
• Weight gain and obesity
• High blood pressure
• Elevated insulin/insulin resistance (IR)/NIDDM
• PCO > 12 cysts 2-8mm diameter (20% XX PCO versus 5-10% XX PCOS)
Diagnosis PCOS exclude - thyroid dysfunction, CAH, elevated PL, androgen-secreting
lesion, Cushing syndrome.
Diagnosis PCOS based 2/3 criteria Rotterdam Consensus 2004 (ESHRE) -
1. USS – PCO> 12 peripheral follicles (ring of pearls) or ovarian volume >10 cm3
2. Oligo- or anovulation/oligo or amenorrhoea
3. Clinical +/or biochemical signs of Hyper-androgenism
LH/FSH raise not a diagnostic criteria (not consistent)
Baseline screening tests exclude other Diagnoses-
TFT, Prolactin, Free androgen index (total testosterone (T)/SHBG x 100= free T).
If free T >5nmol/l –check 17-Ohprogesterone exclude androgen-secreting TU.
Suspicion Cushings Syndrome investigate according to local protocol.
Complications of PCOS - NIDDM, IHD, CVA.
50% PCOS NIDDM/borderline GTT by 40. Hypertension (> 40 yrs).
LDL:HDL cholesterol increased, IHD risk young age – 40% coronary calcification
<45 vs 20% no PCOS , 50% > number of coronary events with PCOS.
Cancer-endometrial hyperplasia & malignancy.
Miscarriage factors

31. PCOS Management
Lifestyle: exercise, weight loss, dietary change
Infertility: Irregular and infrequent ovulation. Ovulation induction
clomiphene 5 days (D2-7/50-100mg), Superovulation (OHSS risk), IVF,
Laparoscopic ovary drill.
Excessive hair growth: Depilatory creams, shaving, waxing,
bleaching, plucking, electrolysis, useful/repeated. Anti-androgen
effect- OCP or Cyproterone acetate reduce hair growth (use min 9
mths). Laser hair removal best long-term method.
Obesity/IR: Obesity profound effect natural/ART conception rate,
also pregnancy complication rate. (>BMI /> IR).
40–50% PCOS overweight: Ovary hyper-androgenism driven by (LH)
slim PCOS, >BMI insulin augments effect LH.
IR present in 10–15% slim/20–40% obese PCOS. Screen- BMI/waist
circumference. If fasting, BG<5.2 mmol/l risk IGT low. 2-hour/75 g
OGTT >risk -BMI> 30 or >25 S.Asia (>IR <BMI).
Metformin inhibits hepatic gluconeogenesis, > insulin sensitivity at
cellular level, direct effect ovarian function. Insulin lowering/ insulin
sensitising agents – metformin, thiazolidinediones (rosiglitazone,
pioglitazone) ? improve symptoms, reproductive outcome. These
drugs unlicensed for PCOS, counsel patients.
PCOS best managed with controlled diet, vigorous exercise and
weight reduction. Orlistat, sibutramine may help reduce BMI and
hyper-androgenism of PCOS. Bariatric surgery may be indicated in
select morbid obesity.
Drug therapy
Metformin, troglitazone - beneficial short-term effect IR
XXPCOS but not DM. Metformin <effect obesity/BMI >35.
Doses 500–3000 mg/day common regime 500TDS or 850BD.
Long-acting agent <GI effects. Metformin not > lifestyle
intervention in improve cardio-metabolic risk/progress T2 DM
Androgen -Metformin may reduce androgen levels by 11%
and modest reduce BMI (>37 BMI poor response).
CVD - No robust evidence prevent CVD in PCOS
Cochrane review – Metformin vs COCP no diff in effect on
PCOS -hirsutism/acne. 20yrs after lap ovarian drill. Persistent
ovulation/norma androgens/SHBG >60% XX (+ if normal BMI)
Health Check
• BP measurement and a fasting blood glucose taken.
• BMI>30 or strong FHx NIDDM OGTT
• All overweight PCOS provide diet and lifestyle advice.
• Amenorrhoeic/severely oligomenorrhoeic PCOS induce
regular (3-4mths) withdrawal bleeds.Reduces risk
endometrial hyperplasia/CA. Cyclical gestogens
(provera/NET at least 12/7), COCP, Mirena® IUS.
• No increase risk Breast CA (routine screen)
• XXPCOS (or partners) ask about snoring/day fatigue
/somnolence risk of sleep apnoea, investigation
/treatment if necessary.
Website: wellbeingofwomen@rcog.or.uk

32. Anatomical Abnormalities of the Genital Tract

33. PAG - Genital tract abnormality
15-years 21/800 adolescents referred
suspected genital tract abnormalities.
18/21 proven congenital tract abnormality,
Causes
6 (33%) Rokitansky Hauser Syndrome (RHS)
6 (28%) Uterine didelphys
5 - Imperforate hymen
3 - Transverse vaginal septum
2 - Septate hymen
1 - Pominent hymenal band
Symptoms
Common
Primary amenorrhoea
Abdominal pain
Other
Urinary retention
Vaginal discharge
Pelvic mass
Difficulty using tampons
Dysmenorrhoea
Delayed puberty
Hirsutism.
Age presentation: Peaks 13-15 years (R 3-16)
RHS presented at younger age, 17% being as young as 7
years. 83% were treated conservatively with progressive
vaginal dilatation, surrogacy/infertility advice, ongoing
review, 17% referred/underwent vaginoplasty.
Uterine didelphys older at median 13 years
40% had a solitary kidney, 20% a non-functioning kidney.
3 cases presented with hemi-obstruction, making
diagnosis more difficult and exemplifying the need for
good diagnostic imaging, paediatric radiologist.
Mullerian agenesis, hypoplasia
Junqueira B L P et al. Radiographics 2009;29:1085-1103
A study of paediatric and adolescent gynaecology services
in a British district general hospital
S McGreal, PL Wood. BJOG 2010; 117(13):1643–1650

34. Lower and upper genital tract - As paramesonephric (müllerian) ducts grow
caudad, reaching the UGS by week 9 (32 mm) and fuse with it to form elevation known
as the müllerian tubercle, with the openings of paramesonephric ducts on either side of
it. A ribbon of epithelium replaces the U-V canal , the precursor of the vagina. Vagina is
formed 16-20th week by development of lacunas; complete canalization later occurs to
form the vaginal lumen. A. Müllerian and wolffian ducts. B. Fusion of müllerian ducts. C.
Regression of mesonephric ducts. D. Uterus, cervix, and vagina.
Embryology – Development Genital tract

35. Type No.
Double ureter, branched, unilateral or
bilateral
15
Hydronephrosis and/or hydroureter 10
Unilateral renal agenesis (all males) 3
Pelvic or “unascended” kidney 7
Horseshoe kidney 3
Bilateral cystic kidneys (both males) 2
Bilateral renal agenesis (both males) 2
Malrotation of kidney (all females) 3
Crossed renal ectopia 1
Urachal cyst 1
Bicornuate uterus (all types) 1
Unicornuate uterus 2
Clitoral hypertrophy 2
Fused labia 1
Absence of external genitalia (sirenomelia) 2
Imperforate urogenital sinus 2
Persistent urogenital sinus 1
Urethra atresia (male) 1
Renal hyperplasia 1
Penile chordee 2
Anomalies of the genitourinary system
From Dougherty CM, Spencer R: Female Sex Anomalies. Hagerstown, MD: Harper & Row, 1972, p. 52.
Because of the close association of mesonephric and paramesonephric ducts,
urinary tract anomalies are frequently associated with malformations of the
external genitalia and vagina.
Thorough urologic studies must be performed on all cases müllerian
anomalies.
Ectopic kidneys and ureters, particularly solitary pelvic kidney, real hazard for
the gynecologist. Renal ectopia per se is not a problem, but if the kidney has
failed to ascend to the normal level, complications can arise.
The short ureter and short blood vessels preclude an attempt to "replace" the
kidney at the normal level.
Incidence solitary kidneys is 1 in 22,000 patients. Associated anomalies of the
reproductive tract are present in nearly all women with a single kidney.
Careful and thorough diagnosis is essential to avoid complications. There are at
least two recorded cases in which solitary kidneys have been removed.
Double ureters may come from solitary kidney does not prove two kidneys.

36. Classification - Mullerian/Uterine Malformations
Incidence: 1 in 200-1 in 600
Diagram vaginal anomalies –
Longitudinal vaginal septum is
the result of failure of lateral
fusion of the Mullerian ducts.
Transverse vaginal septum is
the result of failure in vertical
fusion between the Mullerian
duct and the urogenital sinus
and is usually ipsilateral to the
side of renal agenesis.
American Fertility Society classification 1988 - Müllerian duct anomalies or DES,
∗=uterus may be normal or take variety abnormal forms, ∗∗=may be two cervices.
AFS classification system framework for description anomalies, communication
among physicians, comparison of therapeutic modalities, often confusion about
reporting of certain anomalies, particularly those with features >one class. MRI
gold standard-accuracy, detailed outline uterovaginal anatomy. Laparoscopy and
hysteroscopy reserved for those where interventional therapy may be undertaken.
Incidence Type 111 -Didelphus – 0.1-0.5%

37. MRKH Syndrome (1 in 4500)
Table 1. American Fertility Society classification of
congenital uterine abnormalities (1988)
Class I: Hypoplasia/uterine agenesis
Class II: Unicornuate uterus
Class III: Uterus didelphys
Class IV: Bicornuate uterus
Class V: Septate uterus
Class VI: Arcuate uterus
Class VII: T-shaped uterus results from DES
Mayer–Rokitansky–Küster–Hauser syndrome:
diagnosis and management.
S Valappil, U Chetan, N Wood, A Garden.
TOG 2012;14(2):93-98
MRKH Type 1
Classification – MRKH 3 Types:
1 Typical (64%): Isolated symmetrical UV aplasia/hypoplasia
2 Atypical (24%): Asymmetrical UV aplasia/hypoplasia, absence or
hypoplasia 1 or 2 F tubes. Malform. ovaries +/- renal system
3 MURCS (12%): (mullerian duct aplasia, renal dysplasia, cervical
somite anomalies) syndrome: UV aplasia/hypoplasia, skeletal, renal,
+/- heart malformation.
Associated renal abnormalities (40%): renal agenesis, ectopic or
horseshoe kidney, ectopic ureter
Genetics: sporadic-polygenic/multifactorial inheritance or familial
clustering- autosomal dominant, with variable penetrance, expressivity
of a single mutant gene.

38. MRKH – MRI-blind-end vagina primary
amenorrhea. (A) Sagittal T2-weighted blind-
end vagina (arrowheads), no uterus. (B)
Axial T2 no uterus. Bladder (BL) & rectum
(R) (BO, bowel). R ovary (arrow) normal XX
phenotype.
Didelphys – MRI (A) Coronal STIR
divergent uterine horns (arrows).
(B) Axial STIR x2 cervix (arrows). (C)
Axial STIR caudad to (B) x2 vagina
(arrows) no vaginal obstruction
Partial bicornuate uterus – MRI
2 diverging cornua (arrowheads)
upper 1/3 vagina (V) haematocolpos,
hemorrhagic ovarian cyst (arrow).
(B)haematocolpos. (C) upper 1/3 (V)
full blood, low 2/3 collapsed (*)
arrow thick transverse septum.
Anatomic Anomalies MRI

39. Vaginal Septa Defects
Transverse vaginal septum (pelvic pain/amenorrhea-13 yrs) MRI - (A) Longitudinal US distended uterus (U)/ vagina (V)
haematocolpos (HC); caudal portion of the dilated vagina (arrowheads) not as low as caudal aspect (B) ? transverse vaginal
septum (VS). (B) Coronal T2-weighted fat-suppressed (C) sagittal T1-weighted MRI evaluate for uterine anomalies, normal (U).
(V) and (U) HC. Arrow thick transverse (VS) lower part (V)(*) collapsed. Ovaries noted contain normal follicles (arrows).
Principal congenital anomalies of the vagina include the following
(order frequency):
Longitudinal septum (2)
Transverse septum (3)
Vaginal agenesis (4)
Mesonephric remnants (3)
Hymenal defects (1)
The numbers represent the relative frequencies of these conditions, as
described by Dougherty and Spencer: Female Sex Anomalies. Hagerstown,
MD: Harper & Row, 1972, p. 52 37

40. Longitudinal septums -
“double vagina” complete or incomplete, often with uterus didelphys, many
combinations encountered, including normal uterus /cervix. Sometimes one
cervix may be blocked (retention mucus/ blood). EG usually normal,
septums often not diagnosed unless painful sex or labor dystocia . Simple
incision, ligation bleeding points all that is required. Fistula formation or
vaginal stenosis may result with incautious or extensive surgery. Longitudinal
septums occur x2 frequently as transverse septums.
Transverse septums –
varies occlusion to mild constriction. Frequently, small opening allows
secretions/ blood to drain. Unlike bulging membrane associated with
imperforate hymen, no external sign of blockage. In nearly all internal
organs are normal and pregnancy not infrequent. Transverse septums
represent failure of complete canalization of the vaginal epithelial mass.
Stenosis may be caused by a constricting fibromuscular band. Menstruation
and coitus occur without trouble, condition may not be detected until pelvic
examination reveals its presence.
Symptoms -
Depends on the presence of adequate uterine drainage. Complete vaginal
atresia, lower abdomen mass (hematometrocolpos ), pelvic abscesses, may
cause dystocia and cesarean section the safest method of delivery.
Treatment-
Depends on degree stenosis and rigidity of constricting band. No treatment
or 2/3 longitudinal incisions may suffice. Complete excision of annular
segment of vaginal wall may result in scarring or fistula .
Lesions causing hydrometrocolpos-
A) Imperforate hymen B)Transverse septum C) and D)
Low and high vaginal atresia. Spencer R, Levy DM:
Hydrometrocolpos: Report of three cases review of the
literature. Ann Surg 155: 558, 1962.)
Types vaginal septum

41. Agenesis of the vagina - may only be detected on pelvic examination for
amenorrhea. Always associated with absent hymen. Often misdiagnosed as
imperforate hymen, this is of diagnostic importance. In most cases agenesis
absent/rudimentary uterus +/-ovarian agenesis. Nearly all associated
anomalies urinary tract -renal agenesis, ectopic pelvic kidney, ureteral e
Mechanism not entirely clear; may result failure development epithelial
vaginal mass or failure development UGS.
Treatment- formation artificial vagina is described by Capraro, results
usually excellent if molds are worn regularly or if there is regular coitus.
Imperforate hymen - failure of completion of the canalization or cavitation
of the epithelial plug that fills the vagina. Usually discovered at puberty,
when develops lower abdominal mass, bulging vaginal full of mucus or blood
Treatment – Cruciform incision and drainage under anaesthetic do not
circumferentially excise, may cause stenosis, dysareunia, vestibular pain,
obstruction Bartholin’s ducts leading to cyst/abscess
Pitfalls in diagnosis and management of distal vaginal
agenesis: 10-year experience at a single centre. MG Ugura, O
Balata et al. Euro J Obstet Gyecol 2012;163(1):85-90

42. Congenital Abnormalities of the Vagina
Commonest conditions:
1. Transverse vaginal septum
2. Vertical or complete vaginal septum
3. Vaginal agenesis
4. MRKH
5. Agenesis of the lower vagina
6. Obstructed hemi-vagina with
ipsilateral renal agenesis (OVIRA)
Treatment:
Septal defects: Usually require surgical excision
Creating a neo- vagina:
For vaginal agenesis you need to create a vagina to have normal sexual
function. Length, capacity, lubrication.
Options:
Vaginal dilators (VD): VD pushed against area where vagina should be
located; constant pressure on a daily basis, can create a functional
vagina. Those with vaginal agenesis can have normal orgasms as
clitoris, external genitalia normal. VD takes 6 months-2 years.
Skin grafts: McIndoe procedure, split thickness skin graft (buttock),
space created for the placement vaginal mold with skin graft attached
to it. After seven-days, remove the mold used to create the vagina and
then VD. This can result in a normal, functional vagina. May be dry use
lubricants.
Bowel use: the bowel is used to create a neo vagina. May have chronic
vaginal discharge GI mucosa constantly produces. Concerns exist
about risk STI’s. Prolapse.
Vechietti procedure: Laparoscopic/laparotomy, dissection plane to
hymen, use weighted olive device, placed on traction (see images)

43. Vaginal reconstruction
Ethics - If, in the future ??
Uterine transplantation becomes safe and effective, will it be
ethical for a woman to donate her uterus to her daughter?
With many children awaiting adoption, should women with
Mayer–Rokitansky–Küster–Hauser syndrome be encouraged to
adopt rather than undergo surrogacy?
Who should pay for assisted reproduction treatment, given the
constraints of health service budgets?
Should women with Mayer–Rokitansky–Küster–Hauser
syndrome be managed in selected centres of excellence?
Mayer–Rokitansky–Küster–Hauser syndrome: diagnosis
and management.
S Valappil, U Chetan, N Wood, A Garden
The Obstetrician & Gynaecologist. 2012;14(2):93-98
Ethics - Risks of surgery ?
McIndoe procedure:
Neovaginal space between bladder/rectum lined with split-
thickness skin graft over a mould, inserted into the
neovagina. The woman has to wear the mould for 3 months
and is advised to use a dilator regularly. Disadvantages
vaginal stenosis, perforation bladder/rectum, graft failure,
unsightly scarring the graft site
Sigmoid vaginoplasty:
Disadvantages chronic vaginal discharge, foul odour, stenosis
anastomotic site, risk adenocarcinoma graft
Williams vulvovaginoplasty:
Horseshoe-shaped incision perineum, skin flaps labia majora
create a pouch horizontal to perineum. Technically simpler
than other 2 methods, short length, unusual angle coitus
Most popular techniques:
Vecchietti procedure:
Disadvantages visceral injury laparoscopy, stress incontinence.
Davydov procedure:
Neovagina created peritoneal lining. Dissection rectovesical
space, abdominal mobilised peritoneum, create vaginal
Fornices, attach peritoneum to introitus. Mould worn 6
weeks/regular vaginal dilators

44. PAG Emergencies
• Ovarian cysts – simple (follicular), complex (teratoma)– rupture,
haemorrhage, torsion, acute pain enlarging mass, painful endometrioma.
• Ovarian and or tubal torsion
• Haematocolpos
• Appendicitis (tubo-ovarian abscess)
• Foreign body vaginal/urethra
• Severe menorrhagia (menarche, haematological disorder)
• Acute vulvitis, vaginitis, STI, PID (discharge, systemic unwell, abscess)
• Early pregnancy -ectopic pregnancy, miscarriage, abortion sepsis
• Bartholins cyst/abscess
• Acute congenital anomaly (urinary retention, haematocolpos)
• Labial fusion

45. PAG - Emergencies
Isolated tubal torsion. (A) Color Doppler image shows a swirling appearance
of the vascular pedicle (arrows) and a dilated right Fallopian tube
(arrowheads) with findings concerning for tubal torsion. (B) Corresponding
laparoscopic intraoperative image demonstrates the torsed Fallopian tube.
Detorsion of the Fallopian tube with fenestration of the dilated end
(fimbriaplasty) was performed as the tube and ovary appeared viable
Paraovarian cyst with torsion. Midsagittal US scan through the bladder (B)
shows an enlarged, heterogeneous ovary (arrowheads) and an adjacent cyst
(C). No flow could be elicited on color Doppler interrogation. On surgery it
proved to be adnexal torsion related to a paraovarian cyst leading to
ipsilateral salpingo-oophorectomy.

46. PAG - Emergencies
Ovarian teratoma with torsion. (A) Enhanced axial CT adolescent XX sudden
onset pelvic pain reveals teratoma (arrows) containing fat/calcification.
Adjacent ovary prominent peripheral follicles (arrowheads). Thickened
teratoma wall, surrounding fat is stranded, free pelvic fluid (*). B, bladder; U,
uterus. (B) pathologic specimen; torsion confirmed at surgery.
Bilateral tubo-ovarian abscesses with pyosalpynx. (A) TVUS right adnexa
thick-walled, complex lesion, fluid level consistent with abscess (arrows).
Wall is hyperemic, surrounding soft tissues indistinct/edematous. (B) TVUS
sagittal dilated left Fallopian tube (arrowheads), heterogenous contents,
mucosa thickened consistent with a pyosalpynx. U, uterus.

47. PAG - Emergencies
Foreign body- XX 7 years orange vaginal
discharge. Sagittal T2-weighted. Hypo-
intense cylindrical vaginal structure.
Orange crayon vaginoscopy. (B) bladder
Mature ovarian teratoma- XX 16 years abdominal
pain. (A) X-Ray toothlike calcific density (? Teratoma).
(B) TA-US echogenic adnexal mass (arrows) posterior
acoustic shadowing (arrowheads) ? mature teratoma.
Multitude interfaces near field result from mix
fat/hair obscures rest lesion, “tip of the iceberg” sign
is used. (C) CT large amount fatty tissue in mass
(arrows), typical of mature teratoma. B, bladder.
Perforated appendicitis complicated with
ovarian abscess - XX 13-years. (A) Longitudinal
US enlarged ovary (delineated by cursors) with a
complex collection contains few gas foci
(arrows). (B) US Transverse thick-walled abscess
peripheral hypervascularity. B bladder; U uterus.

48. PAG – Emergencies – Pelvic Pain
XX 18 years acute pelvic pain – TA-US
hemorrhagic ovarian cyst (arrowheads)
with retracting clot. Flow on color
Doppler within the peripheral rim of
normal ovarian tissue (arrows).
XX 17 years acute on chronic pelvic
pain- Sagittal US haemorrhagic cyst
(arrowheads) internal lacy or fish-net
appearance, no flow within septations.
Flow demonstrated in rim normal
ovarian tissue (arrows).
Adnexal endometriosis- XX 17 years (A) Transverse US bilateral adnexal
endometriomas (arrows) internal low level echoes. (B) No flow within lesions
appearances similar to haemorrhagic cyst; (C) Coronal T1 (D) T2 MRI images
adnexal lesions (arrows) high signal on T1/ T2, consistent with blood in lesions.
Left is slightly >heterogeneity/complex appearance B bladder U uterus.

49. PAG Service
Labial adhesions 14% of all cases,
Age:
3 mths-16 years. Peak at 1 year and few after 8 years.
Symptoms:
31% recognised adhesions without prior treatment GP
7% treated by GP care without success
12% urinary symptoms
5% vaginal discomfort
3% vaginal discharge
2% vaginitis
2% vaginal bleeding
Management:
55% conservative active monitoring or discharged
without requiring further treatment.
36% hormone cream alone.
6% division of adhesions using LA/hormone cream
3% admitted as a day case for division under GA
7% re-referred with recurrent adhesions.
PAG - Labial Adhesions

50. Clinical case: Labial adhesions
Management
• Labial adhesions are common in pre-pubertal females may be due
elated to low levels of circulating 0estrogen.
• Small areas of labial adhesions are asymptomatic.
• Interference with urination or accumulation of urine behind the
adhesion can lead to discomfort and symptoms.
• Dysuria and recurrent vulvar and vaginal infections are associated
symptoms. In rare situations urinary retention may occur.
• Asymptomatic labial fusion usually does not require treatment.
• Symptomatic adhesions may be treated with a short course of
oestrogen cream applied twice daily for 7 to 10 days; this may
separate the labia.
• An alternative treatment is to use oestrogen transdermal patches
in close proximity to the labia.
• When medical treatment fails or if severe urinary symptoms exist,
surgical separation of the labia is indicated. This can be done as
an office procedure using 1% to 2% topical Xylocaine gel.
• Because of inadequate levels of oestrogen, recurrences of labial
adhesion are common until puberty.
• Following puberty, the condition usually resolves spontaneously.
Improved hygiene and removal of vulvar irritants may help
prevent recurrences.

51. PAG – Recurrent Vulvo-vaginitis
PAG – Clinic
18% referrals, age peaks bimodal, 4 and 8 years.
Symptoms
44% Vaginal discharge
16% Vaginal soreness
10% Malodour
Recurrent vulvovaginitis or prepubertal vaginal bleeding,
exclude FB (n=5) in this series. These required removal in
either the outpatient or inpatient setting.
Organisms –
41% mixed anaerobes - recurrent vulvovaginitis, no FB
13 % group-B streptococcus
8% candida
7% Haemophilus influenza
3% chlamydia trachomatis
0.5% neisseria gonorrhoea
Bacterial growth by patient age was also bimodal at 4 and 8
years of age, fewer positive cultures with increasing age.
Management - majority were managed conservatively
32% discharged with no action required, family education,
18% actively monitored
17% treated with antibiotics alone
27% were admitted on a day-care basis for a vaginoscopy,
some of whom were also administered antibiotics
3% treated with topical steroids
2% with topical HRT
4% Rate of re-referral for on going vulvo-vaginitis

52. Paediatric/Adolescent Gynaecology –
Common Dermatological Conditions
Pre-pubertal- Dermatitis, Psoriasis, Lichen Sclerosus- three
most common causes vulvo-vestibular rash/pruritus. Poor
hygiene is and intravaginal FB are rare causes. Candidiasis
not seen in non-oestrogenised vulva/vagina. Anti-fundal
cream unhelpful. Infective vulvovaginitis usually Grp A B-
haemolytic strep. Sexual abuse should be considered, but
rarely causes vulval disease. Exclude Pinworm
Vulvo-vaginal rash or pruritus - Most cases atopic/irritant
dermatitis. Rash fluctuates, vulva may be normal. Review
when symptoms are worst. Diagnosis made without tests.
Exam rash is poorly defined (erythema, scale, slight rugosity
labia. Inguinal areas/buttocks affected (?Staph Aureus).
No vaginitis is seen. Vaginal swabs/MSU negative. Green
discharge and no symptoms with (-ve) swab may be normal
variant.
1. Fischer G, Rogers M. Vulvar diseases in children: a clinical audit of 130 cases.
Pediatr Dermatol 2000;17:1-6.
2. Fischer G, Rogers M. Paediatric vulvovaginitis. In: Proceedings of the 3rd
symposium on diseases of the vulva and vagina. Melbourne: Melbourne
University; 1997. p. 26-9.
Psoriasis - Itchy, red, well-demarcated,
symmetrical plaque, no scale. Vulva, perineum,
perianal, natal cleft may be involved. Difficult to
make definite diagnosis, history of cradle cap, bad
nappy rashes, nail pitting, rash behind ear/scalp,
(+) FHx helpful.
Lichen sclerosus - Rare (F>M), familial,
associated autoimmune disease. Intense itchy
vulva, sore, dysuria, bleeding, chronic
constipation. Exam well-demarcated white plaque,
wrinkled , scattered telangiectasia (contact
bleed). Usually figure of eight plaque (vagina and
anus), or any pattern on the vulva, perineum or
perianal area. Vagina is not involved. 2-6%
squamous cell vulval CA adult life.

53. Adolescent
Vulval
Dermatology
Lichen Sclerosus - Note the
“hour-glass” appearance to
the vulva and anus, with
atrophic white center and
surrounding erythema and
hyperpigmentation.
Psoriasis - Confused with contact
dermatitis, candidiasis (intertrigo)
Chronic inflammatory disease of
skin, nails, joints. Age 0- 18 years,
prevalence 1% , incidence 40.8
/100,000 (>1/3 present <18yrs)
Pattern child & adolescent
psoriasis may differ to classical
adult type - face, ano-genital
area. Pruritus common. Look for
other sites- nail pitting, history
severe nappy rash, cradle cap.
Atopic dermatitis - Poorly
demarcated, erythema and skin
fold fissures, non-scaling, spares
creases. Other sites-natal cleft,
angular cheilitis
Psoriasis - diaper area, nail pitting

54. Adolescent Vulvar Dermatology–
Other Conditions and treatment
Other conditions
Streptococcal vulvovaginitis – (Grp A haem strep) acute
vulvitis in a child. Sudden onset erythema, swollen,
painful vulva/vagina, thin mucoid discharge. Preceding
throat infection, or dermatitis. Diagnosed by introital or
perianal swabs. Oral penicillin/cephalexin (10 days to
prevent recurrence).
Foreign bodies - not common (bits toilet paper or fluff),
persistent purulent discharge, may cause maceration
vulval skin. Swabs recurrent bacterial infection, responds
to antibiotics but rapidly recurs, requires EUA and saline
lavage.
Sexual abuse - If concerns about sexual abuse referral to
a paediatrician/child protection unit. Not sure whether a
skin condition or a sign of trauma, refer the child to a
dermatologist.
Treatment
Dermatitis- Avoid contact with soap, bubble bath/shampoo
(use bath oil), tight lycra clothes (wear cotton underwear), no
perfume (toilet paper, wet wipes), avoid OTC medication,
chlorinated water. Apply vaseline or zinc cream before
swimming.
Most respond to 1% hydrocortisone, ointment preferable to
creams (stinging). If resistant consider non-compliance,
infection and psoriasis.
Psoriasis- rash erythematous, well defined, perianal
involvement, look signs of psoriasis, family history.
Lichen sclerosus - white, well-defined eruption. Refer to
dermatologist treating requires potent topical corticosteroid.
Other conditions- Ask if child has been treated for pinworm
infestation.
1. Fischer G, Rogers M. Treatment of childhood vulvar lichen sclerosus with
potent topical corticosteroid. Pediatr Dermatol 1997;14:235-8.
2. Dar V, Roker K.et al. Streptococcal vulvovaginitis in girls. Pediatr Dermatol
1993;10:366-7.
3. Pokorny SF. Prepubertal vulvovaginopathies. Obstet Gynaecol Clin North
Am 1992;19:39-58.
4. Tipton A. Child sexual abuse:. Adolesc Paed Gynaecol 1989;2:10-25.

55. Infectious Vulvo-vaginitis
Management
• Acute vulvar pain, dysuria, and discharge.
• Preceding sore throat.
• The area of inflammation is sharply circumscribed and extends from
the vulva to the perianal area.
• Rosanguineous or grayish-white vaginal discharge, and about one
third have vaginal petechiae.
• Culture of perineal skin and/or discharge is positive. Group B
Haemolytic Streptococcus
• Desquamation ensues with recovery .
• Zinc and Castor Oil Crème. Baths with bath oil
• Oral Cephalexin for 10 days
• Inadequate antibiotic therapy predisposes to recrudescence vulvitis.
• Differential - Impetigo and folliculitis may occur in the vulvar area of
patients of any age and is generally secondary to poor hygiene,
excessive sweating, shaving, or mechanical irritation. Simultaneous
involvement of the buttocks or other skin sites is common. Some
young women with increased androgens, children with a familial
predisposition to keratosis pilaris, and patients with Down syndrome
may be especially prone to developing folliculitis and/or impetigo.

56. PAG - Urogynaecology
Incontinence or urinary symptoms
5% referrals to PAG service.
Age ranged (3-16 years) two peaks were noted
at 12 and 14 years.
Investigations:
Urodynamic studies (3%)
Cystoscopy (3%)
Management:
Antimuscarinic medication (39%), Potassium citrate
(3%)
Prophylactic antibiotics (3%).
Conservative measures:
Caffeine restriction (coca cola)
Bladder training
Urinary input/output charts
Referral:
This group greatest referral rate to other specialities
(17%), included urology, neurology, enuresis clinic,
community/ hospital-based paediatric referrals.
A study of paediatric and adolescent gynaecology
services in a British district general hospital
S McGreal, PL Wood. BJOG 2010; 117(13):1643–1650

57. Sex and the Adolescent
What are the rules?
• In England, Scotland, Northern Ireland and Wales we have to
be 16 or older to have homosexual (gay) or heterosexual
(straight) sex.
• 'Sex' means penetrative sex, oral sex or masturbating
together.
What happens if you have underage sex?
• The law sees it as sexual assault - it's a criminal offence. This
is because in the eyes of the law we are unable to give
informed consent to sex when still a child.
• A boy who has sex with a girl under 16 (17 in NI) is breaking
the law. Even if she agrees.
• If she is 13-15, the boy could go to prison for two years.
• If she is under 13 he could be sentenced to life
imprisonment.
• A girl aged 16 or over who has sex with a boy under 16 can
be prosecuted for indecent assault
What is allowed ?
• There is no law against asking questions. Or finding out
about sex. What it means, how to do it, how to protect
ourselves from the consequences: pregnancy, STIs. And
broken heart.

58. Adolescent Gynaecology – Sex and the Teenager
Use of contraception
• Among 16–19 year olds in 2008–09: 57%
used contraception.
• Of these 65% used condoms and 54% COCP,
86% had heard of EHC
• 17% used EHC at least once in the previous
12 months.
• Use of contraceptive clinic services
• 71,000 women < 16 attended FPC in UK in
2009–10. 7.9% of the resident population, a
slight decrease from 2008–9.
• 281,000 or 21.5% resident female population
in UK aged 16–19 years of age visited a FPC in
2009–10, a slight increase from 2008–09
Sexual Behaviour
The second National Survey of Sexual Attitudes and
Lifestyles (Natsal 2000), which included over 11,000
men and women aged 16–44 in Great Britain:
Median age at first heterosexual intercourse was 16 for
both men and women
One third of men and a quarter of women aged 16–19
had heterosexual intercourse before they were 16
80 per cent of young people aged 16–24 said that they
had used a condom when they first had sex. Less than 1
in 10 had used no contraception when they first had sex
20% men and almost 50% women aged 16–24 said they
wished they had waited longer to start having sex. They
were twice as likely to say this if they had been under 15
when they first had sex.
Both young men and women aged 16–24 had had an
average of 3 heterosexual partners in their lifetime
0.9% men and 1.6% women aged 16–24-year had had
one or more new same sex partners in the previous year
Lader D, Contraception and Sexual Health, 2008/09 (London: Office for National Statistics, 2009).
Information Centre, NHS contraceptive services, England: 2009–10 (London: IC, 2010).

59. Teenage Pregnancies, STI’s and Emergency Contraception
Claim
• Sex education & emergency contraception
causing increase in pregnancy, abortion
and STI’s, in teenagers
Facts
• Teenage pregnancy rates falling
• STI rates increasing (chlamydia & syphilis)
• Syphilis rise due to increase men/men sex
• Only an apparent rise in Chlamydia
• Chlamydia screening programme from 2005

60. Sexually Transmitted Infections
Young people <25 years highest rates of STIs in the UK.
Peak age for STI in women is 19-20 years, and men 20- 23 years.
Of all 16-19 year olds diagnosed with an STI in 2009, at least
11 % women and 12% of men become re-infected within 1 year.
In 2009 there were fewer new cases of gonorrhoea
(3,324/3,452), genital herpes (4,217/4,358) and genital warts
(18,235/18,695) diagnosed in 16-19 year olds than in 2008.
Chlamydia diagnoses in teenagers increased in 2009, from
73,224 in 2008 to 79,720.
These figures include diagnoses made in genitourinary medicine
clinics and in a variety of community settings involved in the
National Chlamydia Screening programme in England.
Health Protection Agency, ‘STI annual data tables’ 2010

61. Pelvic Inflammatory Disease – RCOG Green top guideline no 32- 2008
Adolescence is one of the most important risk factors for STI and PID.
Sexually active they have the highest incidence of any age group.
▪ Chlamydia trachomatis
▪ Neisseria gonorrhoeae,
▪ Mycoplasma genitalium
▪ Anaerobes
▪ Pelvic inflammatory disease
Long-term sequelae of PID include Ectopic pregnancy. Subclinical PID
(chlamydia) is responsible for a significant portion of these long-term
sequelae.
▪ Tubal infertility
▪ Tubo-ovarian abscess
▪ Chronic pelvic pain
2005–UK National Screening Programme for prevention of STI/PID by
screening sexually active adolescents for chlamydial infection. Nucleic
acid amplification assays allow screening self-collected urine or
vaginal swabs. Prevalence Chlamydia is 5-6%, incidence PID 1-2% of
those screened. P Oakeshott et al RCT Chlamydia screening POPI
trial, BMJ 2010.
Symptoms and signs
▪ Bilateral low abdomen tenderness (may radiate to legs).
▪ Abnormal vaginal or cervical discharge.
▪ Fever (greater than 38°C). Abnormal vaginal bleeding
(intermenstrual, postcoital or ‘breakthrough’).
▪ Deep dyspareunia.
▪ Cervical motion tenderness, adnexal tenderness on
bimanual vaginal examination, +/- palpable mass.
Clinical symptoms and signs lack sensitivity and specificity.
PPV of a clinical diagnosis is 65–90% versus laparoscopic diagnosis but
this may also lack sensitivity.
Differential
▪ ectopic pregnancy
▪ acute appendicitis
▪ endometriosis
▪ irritable bowel syndrome
▪ ovarian cyst (rupture/torsion
▪ urinary tract infection
▪ functional pain (unknown
origin).
Tests
▪ TVUS (MRI/CT)
▪ ESR, WCC, CRP
▪ MSU
▪ PID swab screen
▪ ? HIV testing
▪ Contact trace (6mths)
PID Testing -
Gonorrhoea endocervix tested via
culture direct inoculation onto plate
or transport swab by 24 hours or
NAAT. NAAT (+ve) need to swab for
antibiotic sensitivities GN. Chlamydia
endocervix using NAAT Add sample
urethra increases Dx yield GN/CT if
NAAT not available. First catch
Urine/self-taken VV swab for NAAT is
option. (-ve) endocervical/vaginal pus
cells on wet-mount smear good NPV
(95%)/poor PPV(17%) for PID.

62. PID and STIs– RCOG Green top guideline no 32- 2008
PID Treatment
OPD treatment based one following regimes:
▪ Ofloxacin 400 BD + PO Flagyl 400 BD x 14/7
▪ IM ceftriaxone 250 stat, PO doxycycline 100
BD + Flagyl 400 BD x 14/7.
BS antibiotics to cover NG, CT and anaerobes.
Ofloxacin avoid if high risk NG PID due to quinolone
resistance in the UK.
Admission criteria and treatment
▪ surgical emergency cannot be excluded
▪ clinically severe disease
▪ tubo-ovarian abscess
▪ PID in pregnancy
▪ lack of response /intolerance oral therapy
Inpatient treatment should be based on IV therapy x
24 hours until clinically improved then oral therapy.
Recommended regimes:
ceftriaxone 2 g IV daily/ IV doxycycline 100 mg BD
Then PO doxycycline 100 mg BD + Flagyl 400 mg BD
Consideration should be given to removing IUD in
womenwith PID, if symptoms not resolved by 72hrs
Follow-up –
Review at 72 hours - fail to improve needs further
investigation, exclude other diagnoses, may
require admission for IV and or laparoscopy.
Further review 4–6 weeks after therapy ensure:
● adequate clinical response to treatment
● compliance with oral antibiotics
● screening and treatment of sexual contacts
● aware of the significance of PID and its sequelae
● repeat pregnancy test (-ve), if clinical indication
Repeat testing for NG - after treatment in those
found NG(+ve) if sensitivity isolate was not done
Or repeat testing CT and NG if persistent
symptoms, poor compliance, or contact tracing
suggests persistent/recurrent infection.
PID and HIV (+ve) treated with same regimens.
Risk of future PID/requests IUD contraception,
the LNG-IUS would be most appropriate

63. Teenage Contraception and Pregnancy
Wandsworth Guardian
Teenage pregnancies fall across south west London
2:50pm Sunday 11th March 2012 in News
The number of teenage pregnancies has fallen significantly new figures show.
NHS South West London say figures released by the Office for National Statistics indicate
that between 1998 and 2010, most boroughs in the cluster achieved a reduction equally or
surpassing the country's reduction of 24 per cent.
Merton achieved a reduction of 40.4 percent, with both Sutton and Wandsworth achieving
reductions of over 35 percent. These reductions put Merton and Sutton 2nd and 3rd
respectively in a table of the highest reductions in outer London, while Wandsworth is
ranked sixth.
Croydon saw a reduction of 29.3 percent placing them in fourth. Richmond and Kingston also
saw a reduction in line with the national trend. Jonathan Hildebrand, Director of Public
Health for NHS South West London said: "One of the reasons we may be seeing this dramatic
reduction in teenage pregnancy is because of the dedicated work of the Public Health teams
to improve sex and relationship education and access to contraceptive and local sexual
health services.
"There have been a variety of initiatives conducted across the boroughs, for example, Sutton
and Merton commissioned a sexual health service specifically for under 20’s called 'Check it
Out' which offers contraceptive advice and treatment in schools and youth venues. The
boroughs also came together to provide a NHS South West London sexual health website for
under 19s.

64. Teenage Contraception and Abortion
• Under-18 conception ended by TOP increased modestly in the UK
over the past 5 years. Both percentage increases are far lower than
the falls in conception rates.
• The reduction in completed pregnancies driven more by declining
conception rates than rising abortion rates, though both have
contributed.
• The abortion rate in under-18s is double that of women as a whole.
False comparison, since under-18 pregnancies most out of wedlock.
• Compare abortion rate in under-18s with all conceptions outside
marriage, differences less marked. 44.5% of under-18 conceptions
had TOP in 2010, the figure for all conceptions outside marriage for
England/Wales was 30.1%.
• In 2011 number abortions girls <16 years 3,258 vs 3,718 in 2010.
• The vast majority of abortions take place in the very early stages of
pregnancy 79% <10 weeks gestation

65. Uptake Contraceptive Options Female Adolescents
Subgroups of possible interest:
Dual method users
(COCP pregnancy & condoms disease prevention)
HIV positive young women
Sex workers
Teenage mothers
Young married women
Young women from ethnic minority groups
Young women in or leaving care
Young women with learning, physical disabilities
Specific questions are:
What factors do young women say affect their
uptake, choice, discontinuation contraceptives?
What are the mechanisms by which these factors
affect their uptake, choice and discontinuation of
contraceptive methods?
What do they think should be done to increase
contraceptive use and reduce discontinuation?
What do they think should not be done?
Contraceptive options: (excluding abstinence and abortion)
Depo-Provera / Noristerat
Implanon / Norplant
Intrauterine device (IUD) / Intrauterine system (IUS)
Combined pill (oestrogen/progestogen)/progestogen only pill
Diaphragm / cervical cap / spermicide – foam, jelly, cream
Condom / Femidom
Morning-after-pill / Levonorgestrel / Yuzpe regimen
Persona / fertility awareness / rhythm method
Withdrawal / pulling out/ Douch
What are the processes which determine
uptake, choice and discontinuation of
contraceptives among young women,
11-19 years ? (MRC funded study 2006)
What do they think, how do they choose ?
Relationships and rules
Risk behaviour and choices (eg: number of unprotected episodes)
Access to services (and choices made)
Timing of access to services in relation to sexual behaviour
Parental influences on knowledge, attitude and behaviour
Sources of knowledge and sex education

66. Uptake Contraceptive Options Female Adolescents
Conclusions both studies -
Increasing modern contraceptive method use requires community-wide,
multifaceted interventions and the combined provision of information,
life skills, support and access to youth-friendly services. Interventions
should aim to counter negative perceptions of modern contraceptive
methods and the dual role of condoms for contraception and STI/HIV
prevention should be exploited, despite challenges involved.
References:
1. Limits to modern contraceptive use among young women in developing
countries: a systematic review of qualitative research. L M Williamson, A
Parkes, D Wight, M Petticrew, GJ Hart. Repro Health 2009;6(3):1742-55.
2. Accessing Emergency Contraception; the role of friends in the adolescent
experience. D Fallon. Sociology Of Health & Illness. 2010; 32 (5): 677-694
3. Reducing Teenage Pregnancy. D Fallon. Practising Midwife 2010;14(3):23-24.
Salford Adolescent Centred Website
Contraception is free for most people in the UK. With
15 methods to choose from, you'll find one that suits
Contraceptive methods allow you to choose when and if
you want to have a baby, but they don’t protect you from
sexually transmitted infections (STIs). Condoms help to
protect against STIs and pregnancy, so whatever method
of contraception you're using to prevent pregnancy, use
condoms as well to protect you & your partner’s health.
Where to get it
Contraceptive services are free and confidential,
including people under 16 as long as they are mature
enough to understand the information and decisions
involved. There are strict guidelines to for care
professionals who work with people under 16.
You can get contraception free from: most GP surgeries
(talk to your GP or practice nurse), community
contraceptive clinics, some genitourinary medicine
(GUM) clinics, sexual health clinics (these offer
contraceptive and STI testing services), and
some young people’s services (call 0800 567123).
Sexual Health
Many of these places also offer information, testing and
treatment for STIs. If you've been exposed to the risk of
pregnancy, you're also at risk of catching an STI.
Before you make an appointment, make sure you’re as
informed as possible about the contraceptive options
available. People’s choice of contraception may vary over
time, depending on their lifestyle and circumstances.

67. Emergency Contraception

68. Cervical Screening and HPV Vaccination
Two current HPV vaccines: Gardasil and Cervarix protecting against
HPV-16 /HPV-18, cause 70% of cervical, 80% anal, 60% vaginal, 40% of
vulvar cancers. Gardasil prevents HPV-6 /HPV-11 cause 90% genital
warts. Worldwide, HPV is the most common STI and is a cause of CIN.
WHO vaccination of young women against HPV to prevent squamous
cervical cancer/reduce CIN treatments. HPV vaccines may also reduce
adenocarcinoma. Regular Pap smears are required even after vaccine
as there are other high-risk HPV types. Protection from HPV 16/18
lasts 5 years for Gardasil, > 6 years for Cervarix. Booster vaccines may
not be necessary.
Since September 2008 there has been a UK national programme to
vaccinate girls 12-13 years (year 8) against HPV
Cervical Screening
Between 25-60 years the NHS cervical screening
programme contacts you every 3-5 years for a
smear test. 3 yearly screens prevent 84/100 cancers
that would develop with no screening.
Diagnostic screening of symptomatic young
women still indicated (risk assess)

69. Adolescent Gynaecology and Psychiatry
• Psychological, physical and sexual abuse - vulnerability
• Eating disorders
• ‘Depression’ – symptoms and syndromes
• Body dysmorphic disorders
• Munchausen by proxy
Psycho-social development -awareness of family dynamics,
(parents and siblings), friendships, social, school, other
external activities, the role of social media.

70. Body Dysmorphic Disorders (BDD)
Somatoform disorder, preoccupation with imagined or trivial defect in appearance.
Exclude other disorders eg. weight concern (eating disorder)
1-2% world population meet criteria for BDD, risk male=female, rarely in children.
Causes are a combination of biological, psychological, environmental factors.
Psychological trauma stemming from mental, physical abuse or emotional neglect,
can contribute to a person developing BDD.
Preoccupation with body image occurs in adolescence or early adulthood, self-
criticism of personal appearance, develops atypical aesthetic-standards with
discrepancy between internal perception of ‘actual’ and ‘ideal self’.
BDD symptoms include depression, social phobia, and OCD. Affected individual may
become hostile towards family members for no reason.
Diminished QoL, can be co-morbid with major depressive disorder and social phobia
(chronic social anxiety); suicidal ideation 80%, extreme cases linked to dissociation
Treatment successful with CBT and SSRIs

71. Adolescents and the Designer Vagina
Hundreds of girls aged 14 or under are
having 'designer vagina' surgery on the
NHS. 343 operations performed on
under 14s in six years
Researchers want an age limit for the
surgery . PUBLISHED:22 November 2012
Trend: Hundreds of girls are having
'designer vagina' surgery on the NHS, say
researchers from UCHL, led by Dr Sarah
Creighton, claim it is ‘disturbing’ that
there is no minimum age limit for the
surgery.
Websites of companies make
'Unsubstantiated claims of physical,
psychological and sexual benefits were
present on every website’. Labiaplasties,
operations to reshape the labia, the
inner lips of the vagina, have become
increasingly common……. ‘Given the fact
that anatomy continues to change
throughout the lifespan, the younger a
girl begins her FGCS journey the higher
the number of lifetime operations and
the greater and more multiple the risks’
she said.
This picture is showing a part of art piece, The great wall of vaginas, which was created by a
British artist Jamie McCartney. Nine metres long wall of 400 volunteer women’s private
areas sculptured from many different countries between the ages of 18 to 76. With the large
increment in cosmetic labial surgeries, he hopes this sculpture can lead people to understand
that vulvas and labia are as different as faces . There is no “perfect” vagina.
Techniques:
Mark labia surgical pen and
agree labial outline and shape.
Trimming labia
Wedge excision (hypertrophy)
Z plasty (very large ‘bat wings’)

72. Adolescent genital surgery - designer vagina or mutilation?
Types surgery ?
• Labia reduction surgery or labioplasty
• Hymenoplasty or hymenorrhaphy
• Other forms of female cosmetic genital surgery
– Revirgination refers to surgery for vaginal ‘laxity’,
believed to result from childbirth and/or ageing.
– G-spot amplification consists of injections in the
area G-spot is purported to be to enhance sexual
arousal/pleasure during sex
How to respond to requests for female genital cosmetic surgery ?
1. Be sensitive when taking a history.
2. Ask about her ideas, concerns and expectations.
3. Ask about child sex abuse/domestic/other physical violence.
4. Ask whether she’s been taunted about genitals by a sexual partner.
5. Examine and reassure her regarding normality/variation.
6. Show pictures of normal female external genitalia.
7. Explain risks/complications/potential damage to long-term function.
8. Consider referral to a psychologist.
Female genital cosmetic surgery: how can clinicians act
in women’s best interests?
Michala L, Liao LM, Creighton SM. TOG 2012;14:203–206.

73. Forensic and Legal Aspects to Adolescent Gynaecology
Duty of care
• Requirement for parental/guardian consent
• Contraception/sexual health issues/termination of pregnancy
• Suspected sexual abuse/assault
• Age of consent sexual intercourse
• Who to inform and when to inform – social work, police, forensic team ?
Role paediatric/adolescent forensic evaluation team
Haven Clinics and similar services
Child protection officer
Safeguarding Children team
www.thehavens.co.uk/

74. Organisation of the Adolescent Clinic
Burack 2000
• Questionnaires 13-15 years
attitudes towards GP and sexual
health services
• Majority believed you had to be
over 16 years to access and were
worried about confidentiality
Court 1993, Donovan 1997
• Degree of informality and optimal
waiting room conditions
• No appointment delays
• Staff friendly
• Continuity of care with same doctor
• Personality doctor important
Quadrel and Low 1990
• Attitudes of teenagers (late teens)
to their doctor is closely linked to
parental views
• Take patients and parents feedback
on board
Special needs of the patient ?

75. Recommendations for
Adolescent Gynaecology Practice
• Make the adolescent central to the
consultation
• Respect privacy maintain confidentiality
• Take great care over examination always
obtain consent
• Provide clear explanations
• Be aware of parents concerns and address
if possible
• Help adolescents take responsibility for
their own health
Adapted from J MacDougall
Paediatric and Adolescent Gynaecology: A Multidisciplinary Approach
Consultation and setting
Communication skills
Adolescent needs acknowledged
Examination and consent
Summing up
Robin Bush Adolescent Clinic

76. Adolescent Gynaecology
Consent for Treatment
Conditions that encourage young people to be competent and contribute to
decision making -
The presence of Free from Understanding Able to
Supportive-affectionate
parent-child relationship
Pressure There is a decision to be made Retain an understanding
Trust and confidence in the
doctor-patient relationship
Panic Decisions have consequences Appreciate importance
Adequate information
presented in an appropriate
way
Pain Nature of recommended
intervention and alternatives
See how it applies to them
Other ‘temporary’
factors impairing
judgement
Risk versus benefits of
intervention or no intervention
Weight the issue in the
balance
Short-term and long-term
consequences
Adapted from Shaw et al 2001

77. Still interested?
• Suggested reading
• Further training
• Careers
www.britspag.org/

78. Adolescent Gynaecology
Review objectives
✓Overview normal physiological development; skeletal growth, maturation of
the reproductive tract, development secondary sexual characteristics, CNS
maturation, personality and psychology of the female adolescent.
✓Adolescents presenting with Specific Gynaecology issues:
✓Menarche and physiological changes
✓Congenital disorders
✓Adolescent gynaecological disorders
✓Problems unique to adolescents,
✓General gynaecological disorders presenting in adolescents
✓Adolescent urogynaecology
✓Haematological disorders presenting with secondary gynaecological symptoms
✓Dermatological conditions presenting with gynaecological symptoms
✓Sex and the adolescent - STD’s, PID, cervical screening, HPV vaccination
✓Teenage Contraception and Pregnancy
✓Adolescent gynaecology and psychiatry - Body dysmorphic disorders
✓Forensic and legal aspects to adolescent gynaecology