Adolescent Gynecologic Care

QUESTIONS 1, 2, 3

The latest recommendations from the American College of Obstetrics and

Gynecology (ACOG) and the American Cancer Society state that women should
NOT have first Pap smears until the age of 21 years (SOR A; Ref. 1). This
recommendation is based on the low likelihood of cervical cancer in younger women and
the growing body of evidence of harm from aggressive treatment for precancerous lesions.
Further, the American Society for Colposcopy and Cervical Pathology (ASCCP) has
presented guidelines for managing abnormal cytology in adolescent women (under the age
of 20 years) who received a screening Pap smear contrary or prior to the new guidelines.
These recommendations are much less aggressive than previous practice and involve
observation and rescreening except in some cases of high-grade lesions. For example, in
adolescent women with atypical squamous cells of undetermined significance (ASCUS) or
low-grade squamous intraepithelial lesion (LSIL) on their Pap smear, the new
recommendation is to repeat cytology at 12 months. Colposcopy is only recommended if
abnormality persists for 24 months or if the initial repeat Pap smear at 12 months is highgrade dysplasia.
Human papilloma virus (HPV) is very common among adolescents. Studies have shown
positive HPV testing in as many as 50% of sexually active young women within the first 3
years of the onset of sexual activity. Prevalence of HPV in sexually active adolescents in
the U.S. is estimated to be up to 57%. Within 24 months, 90% of adolescent women will
clear the infection. For this reason, screening adolescent women for HPV is not
recommended. HPV vaccine (Cervarix or Gardasil) is recommended in females aged 11-12
years but can be given to young women up to age 26 years. Cervarix is a bivalent vaccine
for protection against HPV types 16 and 18, the subtypes of HPV most likely to cause
precancerous cervical changes. Gardasil is a quadrivalent vaccine with additional protection
against HPV types 6 and 11, the most common types causing genital warts. Adolescents
should be warned about the potential increased risk of oral cancers associated with HPV.
Many adolescents feel that oral sex not really "sex" and is without risk.
Sexually active adolescents are at increased risk of developing sexually transmitted
infections (STIs). In the U.S., reported rates of Chlamydia trachomatis and gonorrhea are
highest in young women ages 15-19 years. These infections are more prevalent in
adolescent women who have multiple sexual partners or sequential short-term sexual
partners and who fail to use condoms regularly and appropriately. Young women also have
a higher biological susceptibility for STIs. Chlamydia or gonorrhea infection can have longterm consequences by causing pelvic inflammatory disease (PID) and future infertility. All
sexually active females under the age of 25 years should be screened annually
for C. trachomatis and gonorrhea (SOR B; Ref. 4). In asymptomatic women, a
speculum examination is not necessary to diagnose these two infections and may actually
be a barrier to adolescents receiving care. Urine screening for chlamydia and gonorrhea is
appropriate. Adolescents who have pelvic symptoms (e.g., vaginal discharge, abdominal or
pelvic pain) should be evaluated with a speculum examination and a bimanual
examination. STI testing can be performed in adolescent women without parental
permission.
Weight, blood pressure and a careful health history (including medical history,
menstrual history and family history) are all that is required to safely prescribe
combined oral contraceptives (COCs) (SOR C; Refs. 6, 7). Pelvic examinations are
not required and may actually be a barrier for adolescents to discuss pregnancy
prevention. Neither irregular nor heavy menses are contraindications to COCs. In fact,
COCs will likely improve these menstrual problems. However, if the young woman does not
understand the directions regarding COC use, she should not receive a prescription. No
clinical breast examination should be performed.
A 2009 ACOG Committee Opinion recommends that clinicians make every effort to
encourage adolescents to use long-term, user independent methods of contraception due
to their efficacy and the ease of use. Both intrauterine contraceptive devices (IUDs)
ParaGard and Mirena; and the contraceptive implant (Nexplanon) are appropriate to use in
adolescents. ACOG further encourages the use of same-day insertion protocols (rather
than waiting until the next menses) since inserting an IUD or implant on the same day of
the visit will eliminate the risk of pregnancy during the interval until the next menstrual
period.

Delayed Puberty Questions 4-8

Constitutional delay of puberty (first question) is the most common cause of delayed
puberty, especially in boys. The characteristics of constitutional pubertal delay are
short stature (resulting from a decrease in growth velocity in the first few years
of life), delayed puberty and delayed epiphyseal maturation. There is often a family
history of "late bloomers." Affected children usually have a relatively short upper body
segment but are otherwise healthy. Although there is a delay in the onset of puberty, the
sequence of pubertal development is normal. The delayed epiphyseal maturation is
consistent with the extent of pubertal maturation. Current evidence suggests that there is
a physiologic delay in the maturation of the central nervous system that results in a delay
in the normal decrease in the sensitivity of the hypothalamic-pituitary axis to the
prepubertal levels of the sex hormones. There has also been a suggestion that a delay in
the initiation of the unique pubertal hypothalamic-pituitary, sleep-associated luteinizing
hormone secretory pattern is a cause of constitutional delay of puberty. It is sometimes
very difficult to differentiate constitutional delay in puberty from isolated gonadotropin
deficiency, especially in the early teenage years. In constitutional delay of puberty, short
stature and slow growth velocity correlate well with bone age, and there is also a delay in
adrenarche (adrenal gland maturation manifested as pubic hair development and
sebaceous gland development). In contrast, children with isolated gonadotropin deficiency
usually have normal stature and there is no effect on adrenarche. The Table contains the
differential diagnosis for short stature.

Causes of Short Stature in Children

Eating disorder: anorexia

Failure to thrive

Growth failure

Growth hormone deficiency

Hypopituitarism

Hypothyroidism

Genetic short stature

Laboratory tests to consider when evaluating a child for short stature include

Complete blood count (CBC), liver function tests and erythrocyte sedimentation
rate (ESR) to rule out systemic conditions

Thyroid-stimulating hormone (TSH) and serum free thyroxine (T4) to rule out
hypothyroidism caused by thyroid, hypothalamic or pituitary conditions

Serum prolactin to rule out hyperprolactinemia that can delay puberty

Serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH)

(gonadotropins) along with estradiol in girls and testosterone in boys to
distinguish between primary (high LH and FSH) and secondary (low LH and FSH)
hypogonadism; gonadotropins will typically be low in constitutional delay of
puberty and congenital gonadotropin-releasing hormone (GnRH) deficiency
Depending upon the results of the tests above, consider adrenal androgen measurement,
especially dehydroepiandrosterone sulfate (DHEA-S). DHEA-S is more likely to be normal
in cases of congenital gonadotropin-releasing hormone (GnRH) deficiency than in cases of
constitutional delay of puberty, although the expected values overlap.
Often, only time and serial observations can distinguish between congenital GnRH
deficiency and constitutional delay of puberty. Fortunately, the latter is much more
common, accounting for more than half of all cases of delayed puberty, and requires no
intervention other than reassurance of the patient and family. If no signs of puberty
appear by age 14 years in boys and 12 years in girls, consideration for further
specialized evaluation and hormone administration is appropriate (SOR C; Ref.
3).
Testicular feminization syndrome (second question) patients are genetically male but
appear phenotypically female. The disorder is due to a mutation or structural abnormality
of the androgen receptor gene with resultant resistance to the action of androgen at the
cellular level. Affected patients have female body habitus and psychosexual orientation. At
puberty, estrogenic steroids secreted by the testes bring about development of the
breasts. Pubic and axillary hair are absent or sparse. Menstruation, however, does not
occur. The vagina ends blindly in a pouch and the uterus is absent. Gonads show Leydig
cell hyperplasia with defective spermatogenesis. The gonads may present as inguinal
masses and may undergo malignant changes if orchiectomy is not performed by late
adolescence. More than 50% of affected patients have an inguinal hernia. Patients with
testicular feminization syndrome have an elevated concentration of serum testosterone for
age. Treatment for patients who are phenotypically female and have been raised
as girls is estrogen administration (SOR C; Ref. 5).
Klinefelter syndrome (third question) is the most common cause of primary testicular
failure in males. Affected patients have a karyotype of 47 XXY. Klinefelter syndrome occurs
with an incidence of approximately 1 in 500-1,000 males. The pubertal delay is caused by
seminiferous tubule hyalinization in the testes with absence of spermatogenesis. Affected
patients have a slowing or arrest of pubertal development as testicular function declines.
Secondary sexual characteristics often do not progress. Characteristic features include tall
stature with relatively long arms and legs, micropenis, small testicles, infertility,
gynecomastia and borderline IQ. There have been reports of fertility in mosaic patients.
Other features include prognathism (protrusion of the jaw), epicanthal folds, hypertelorism
(widely spaced orbits), strabismus, scoliosis and radio-ulnar synostosis. Affected children
may be either excessively shy or aggressive, have poor social adaptation and may engage
in antisocial acts. Occurrence of more than 2 X chromosomes may result in Klinefelter
variants. In general, the greater the number of X chromosomes, the higher the frequency
and severity of mental retardation and somatic features. Diabetes mellitus, breast cancer
and osteoporosis occur with increased frequency in patients with Klinefelter syndrome.
Serum gonadotropins increase to castrated levels by early adolescence. Treatment
involves administration of testosterone to achieve secondary sexual
characteristics (SOR C; Ref. 5).

Inhalant Abuse Qs 9-10

Inhalant abuse is a significant health problem, occurring most commonly in young

adolescents. A 2009 survey in the U.S. found that 2.1 million persons >12 years of age
abused inhalants. A 2010 study found that 8.1% of 8th graders, 5.7% of 10th graders and
3.6% of 12th graders reported abusing inhalants at least once in the year prior to the
survey. These statistics are similar to other studies, indicating that inhalant use is most
common in young adolescents and that inhalant abuse diminishes with age. Many
of these youths transition to other drugs and/or alcohol (SOR C; Refs. 2, 3).
Overall, 9% of persons >12 years of age report using an inhalant for its psychoactive
properties at least once. Hispanic and white students are twice as likely to use inhalants as
black students. Risk factors for inhalant abuse include low level of parental education,
having dropped out of school and lack of intention to complete college. Inhalants are legal,
easy to obtain and inexpensive making them the entry drug of choice for young teens.
Inhalant abuse may involve a large number of products. (See first Table.) Chemicals
contained in these products include toluene, butane, propane, fluorocarbons and acetone.

Commonly Abused Inhalant Products

Agents
Airplane glue
Glues and adhesives
Users employ several methods
Other to
glues
abuse these products. (See next Table.) Inhalation
results in rapid pulmonary absorption. High lipid solubility of the compounds results in
spray
rapid neurological effects Cooking
euphoria,
stimulation and disinhibition. Other effects may
Spray
paint
develop within seconds or minutes, including dizziness, slurred speech, drowsiness, slowed
spraysniffing death syndrome is probably due to cardiac
thinking and disorientation.Hair
Sudden
Aerosols
Deodorant
arrhythmia, because inhalants interfere with electrical conduction. Injuries and deaths also
Air freshener
result from
risky behaviors due to disinhibition.
PC and video head cleaners

Solvents and gases

Paint remover and thinner

Nail polish remover
Lighter fluid
Fire extinguisher
Correction fluid and correction fluid thinner
Gasoline
Varnishes, lacquers, resins

Cleaning agents

Spot remover
Degreaser

Methods of Inhalant Abuse

Description
Sniffing or snorting
Bagging*
Huffing*

Direct inhalation of fumes

Numerous adverse effects result from chronic inhalant use. (See last Table.) Early
Breathing
fumes
from aor
plastic
or paper
detection and intervention
may help
to prevent
minimize
thesebag
adverse effects.
However, there is no associated
risk
of
metabolic
alkalosis,
cholelithiasis
Soaking a cloth with the inhalant and puttingor oropharyngeal
cancer.
cloth over nose
or mouth

Dusting

Directly spraying aerosol cleaners into nose or

mouth

Glading

Directly spraying air freshener into nose or

mouth
*Preferred methods due to the high concentration of inhalant that can be obtained

Adverse Effects of Chronic Inhalant Abuse

Effects
Motor, cognitive, sensory defects; learning
Signs and symptoms of acute
inhalant
use may be
subtle or absent because the
and memory
impairment;
Parkinsons
Neurologic
drug effects are brief. Treatment
disease; damage
of acute
to cerebellum
inhalant intoxication
(impaired
is primarily
supportive (SOR C; Ref. 1).
Chronicand
users
may have the
inhalant odor on their breath or
strength
coordination);
peripheral
clothing; perioral or facial rashes
neuropathy;
(dryness
optic
and
nerve
erythema,
damage
eczematoid) may also occur.
Treatment of chronic inhalant abuse requires a different focus than other forms of
Conduction
cardiomyopathy,
substance abuse because those
affected abnormalities,
are generally younger.
There are few studies that
Cardiopulmonary
dyspnea,
emphysema-like
changes,
specifically address treatment modalities for inhalant abuse,
and few specialized treatment
reactive
airways
programs exist. A Cochranepneumonitis,
review foundasthma-like
no high-quality
studies
regarding treatment.
Current interventions include
education,
counseling,
treatment
of
associated anxiety or
Renal tubular acidosis, glomerulonephritis,
Renal
depression, and addressingcalculi,
psychosocial
issues
(including family dysfunction, which is
metabolic
acidosis
common).
Digestive
Hepatitis, anorexia, weight loss
Physicians should ask youngAplastic
adolescents
about
inhalant use
and educate them about the
anemia,
malignancy
(leukemia,
potential dangers. Educating
parents
about
the
abuse
potential
of common household
lymphoma, multiple myeloma)
products may also be helpful.
Menstrual abnormalities; pregnancy
complications (preeclampsia, spontaneous
Reproductive (women)
loss), fetal effects in pregnancy similar to
fetal alcohol syndrome
Hematologic

Psychosocial

Poor self-esteem, suicidality, poor school

performance, criminal behavior, adjustment
disorders