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PELVIC ORGAN PROLAPSE
83
B
iBliography
1. American College of Obstetricians and Gynecologists. Pelvic organ prolapse. ACOG practice bulletin no. 85. Obstet
Gynecol. 2007;110:717–729.
2. Bradley CS, Zimmerman MB, Qi Y, Nygaard IE. Natural history of pelvic organ prolapse in postmenopausal women.
Obstet Gynecol. 2007;109:848–854.
3. Bump RC, Mattiasson A, Bø K, et al. The standardization of terminology of female pelvic organ prolapse and pelvic
floor dysfunction. Am J Obstet Gynecol. 1996;175:10–17.
4. Culligan PJ. Nonsurgical management of pelvic organ prolapse. Obstet Gynecol. 2012;119:852–860.
5. DeLancey JO. Anatomy and biomechanics of genital prolapse. Clin Obstet Gynecol. 1993;36:897–909.
6. Haylen BT, de Ridder D, Freeman RM, et al. An International Urogynecological Association (IUGA)/International
Continence Society (ICS) joint report on the terminology for female pelvic floor dysfunction. Neurourol Urodyn.
2010;29:4–20.
7. Khan AA, Eilber KS, Clemens JQ, et al. Trends in management of pelvic organ prolapse among female Medicare
beneficiaries. Am J Obstet Gynecol. 2015;212:463. e1-e8.
8. Richter HE, Burgio KL. Stress urinary incontinence and pelvic organs prolapse: nonsurgical management. In: Walters
MD, Karram MM, eds. Urogynecology and Reconstructive Pelvic Surgery. 4th ed. Philadelphia: Saunders; 2015:249.
9. Sung VW, Hampton S. Epidemiology and psychosocial impact of female pelvic floor disorders. In: Walters MD, Karram
MM, eds. Urogynecology and Reconstructive Pelvic Surgery. 4th ed. Philadelphia: Elsevier; 2015:96–104.
10. Walters MD, Ridgeway BM. Surgical treatment of vaginal apex prolapse. Obstet Gynecol. 2013;121:354–374.
11. Walters MD, Unger CA. Description and classification of lower urinary tract and pelvic organ prolapse. In: Walters MD,
Karram MM, eds. Urogynecology and Reconstructive Pelvic Surgery. 4th ed. Philadelphia: Saunders; 2015:109.
Table 18-3. Surgical Treatment for Pelvic Organ Prolapse
TYPE OF PROLAPSE SURGICAL OPTIONS
Anterior vaginal wall Anterior colporrhaphy (“anterior repair”)
Paravaginal defect repair
Apical Transvaginal:
Uterosacral ligament suspension
Sacrospinous ligament fixation
McCall culdoplasty
Colpocleisis*
Transabdominal:
Sacrocolpopexy (via laparotomy or laparoscopy)
Posterior vaginal wall Posterior colporrhaphy (“posterior repair”)
Site-specific repair
*Obliterates the vaginal canal
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1. How is the breast examination performed?
In general, be methodical and consistent. Palpation should be systematic and with variable pressure.
Examine the patient while she is in the sitting and supine positions. Have the patient flex the pectora-
lis muscle to look for any skin retraction or dimpling. The areola should be compressed to identify any
discharge as well as to evaluate for nipple retraction. To evaluate for lymph nodes, ask the patient to
open the axilla by placing the ipsilateral hand behind her head.
2. What physiologic changes occur in the breast during the luteal phase of the
menstrual cycle?
Cyclic symptoms of increased sensitivity, pain, or even nipple discharge result from an increase in
size, nodularity, and density. Breast volume increases an average of 25 to 30 mL. Breast examination
is therefore best performed shortly after menses.
3. How common is breast pain (mastalgia)?
Breast pain occurs in more than two thirds of menstruating women. Cyclic pain tends to be diffuse,
bilateral, and associated with benign fibrocystic changes. Noncyclic breast pain is localized and
may be associated with an identifiable cyst or mass. Pain alone is rarely a presenting symptom of
malignant disease. Various treatments have been used for mastalgia and include analgesics, low-dose
diuretics, danazol, and reduced caffeine intake.
4. What is mastitis?
Mastitis refers to the inflammation of breast tissue. It can be categorized as infectious or noninfec-
tious. Noninfectious mastitis may warrant workup for possible malignancy. Lactational mastitis
occurs in 2% to 10% of breastfeeding women and manifests with fever and a tender, red, engorged
breast. Treatment is directed against Staphylococcus aureus (including methicillin-resistant S. aureus
[MRSA]), and women are encouraged to continue breastfeeding.
5. What is galactorrhea, and what are common causes?
Galactorrhea refers to spontaneous milky, nonbloody discharge from the nipple. It results from
increased prolactin levels. Dopamine exerts negative feedback on prolactin release, and thyrotropin-
releasing hormone (TRH) promotes prolactin release. Therefore, medications that have dopamine
antagonist activity (e.g., antipsychotics or other phenothiazine drugs) or conditions in which the
patient would have high levels of TRH (hypothyroidism) can cause galactorrhea. Pregnancy, oral
contraceptives, and prolactinomas can also cause galactorrhea.
6. What is the most common cause of bloody nipple discharge?
Bloody discharge is most commonly the result of a breast neoplasm, and the most frequent neoplasm
is a benign intraductal papilloma.
7. What are fibrocystic changes of the breast?
Fibrocystic changes are the most common benign breast conditions. They are characterized by fibro-
sis of breast stroma and the formation of cysts, and they typically affect women of reproductive age.
Some women can palpate changes in the breast, but most women with fibrocystic change experience
cyclic breast pain. Fibrocystic changes are not associated with an increased risk of breast cancer.
8. How should a mass be described?
Size, contour, consistency, and mobility should be noted, along with any attachment to skin or
underlying fascia. Careful examination of the axillary and supraclavicular lymph nodes should also be
performed, and any nipple discharge or rashes should be noted.
9. What is the differential diagnosis of a breast mass?
Breast cancer, fibrocystic disease, fibroadenoma, and trauma (fat necrosis); the frequency varies with
age. Fibrocystic change is the most common cause of a breast mass.
CHAPTER 19
BREAST DISEASE
Susan Park, MD
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10. What important information should be obtained from a patient being evaluated for
a breast mass?
Most newly discovered breast masses are found by the patient herself. It is important to ask when the
mass was first found, how it has changed, whether it changes with the menstrual cycle, and whether
it is painful.
11. What characteristics of a breast mass suggest malignancy?
Palpable breast cancers usually have irregular or indistinct borders and may be attached to the skin,
dermal attachments, or underlying fascia. More advanced local disease produces skin changes that
result in retraction, dimpling, induration, edema (“peau d’orange”), ulceration, or inflammation. How-
ever, no physical characteristics can reliably distinguish between benign and malignant lesions—any
breast mass should be examined by biopsy.
12. What are the risk factors for breast cancer?
Carcinoma of the breast, the most common malignant disease in women, occurs in 12% (1 in 8) of
women during their lifetime. Risk factors include age, family history of breast cancer, history of breast
cancer in the opposite breast, combined estrogen and progesterone hormone therapy (HT), early
menarche or late menopause, nulliparity, radiation exposure, and a history of colon or uterine cancer.
The Gail model is a computer model that combines various risk factors to produce an individualized risk
assessment. It does not, however, include whether a woman has been tested for BRCA genes or used HT.
13. What are the BRCA genes, and why are they important?
The breast and ovarian cancer genes BRCA1 and BRCA2 are found on two separate chromosomes.
The lifetime risk of breast cancer in women with these mutations may be as high as 85%, and
the lifetime risk for ovarian cancer is 20% to 40%. Women with a strong family history of breast or
ovarian cancer may choose to be screened. Women who test positive require increased surveillance
for cancer and are offered prophylactic mastectomy or oophorectomy after childbearing has been
completed.
14. Does the use of HT increase a woman’s risk of breast cancer?
According to the Women’s Health Initiative (WHI), which was a large cohort study of women receiving
HT after menopause, the risk of breast cancer (relative risk [RR]: 1.24; confidence interval [CI]: 1.02
to 1.5) is slightly increased with the use of a combination estrogen-progesterone regimen but not
with estrogen alone. (The estrogen-only arm of the study actually showed a statistically insignificant
decrease in risk, with an RR of 0.8 [CI: 0.62 to 1.04]). Women should consider their baseline risk of
breast cancer before they take HT. A family history of breast cancer does not in itself preclude the
use of HT.
Oral contraceptives have not been shown to increase the risk of breast cancer.
15. Is there anything a woman can do to reduce her risk of developing breast cancer?
For women at average risk, no proven methods exist because most of the risk factors (e.g., family his-
tory, age at menarche) are not able to be modified. For women at very high risk, tamoxifen has been
shown to reduce the incidence of new hormone receptor–positive breast cancers. It has not, however,
been shown to reduce deaths or the risk of hormone receptor–negative cancers. Prophylactic
oophorectomy has been shown to decrease breast cancer risk by 50%, and prophylactic mastectomy
decreases breast cancer risk by 90%.
16. What are the current breast cancer screening guidelines?
Mammography screening is associated with a 19% overall reduction of breast cancer mortality (≈15%
for women in their 40s and 32% for women in their 60s), but it has disadvantages of false-positive
results and overdiagnosis. At this time, a discrepancy exists among major organizations regarding
breast cancer screening. Recommendations from the American Cancer Society, the American College
of Obstetricians and Gynecologists, and the U.S. Preventive Services Task Force are summarized in
Table 19-1. Screening magnetic resonance imaging (MRI) scans should be reserved for high-risk
(>20%) women such as BRCA carriers.
17. What initial diagnostic step should be taken to evaluate a newly discovered
mass?
A diagnostic mammogram should be the first imaging study to be performed, even if a patient has
had a recent negative mammogram. Ultrasound can be used to determine whether a mass is solid or
cystic, and it is the first-line imaging method for a woman who is pregnant or lactating.
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GENERAL GYNECOLOGY
18. If a breast cyst is aspirated, should the fluid be sent for microscopic examination?
Only if it is bloody. Clear or yellow fluid does not need to be sent for cytologic analysis.
19. What characteristics of an aspirated cyst require further workup?
Aspiration of bloody fluid or a residual mass remaining after aspiration. Further diagnostic studies
should also be performed if a cyst recurs.
20. What are the advantages and disadvantages of fine-needle aspiration (FNA) of a
breast mass over a core or excisional biopsy?
Confirmation of any breast mass is made by either FNA or core biopsy. FNA is easily and safely
performed in an office or clinic setting. It distinguishes cystic from solid masses and provides cells for
subsequent cytologic evaluation. However, it requires considerable skill to obtain a satisfactory sample
and has significant false-negative and false-positive rates. A core or excisional biopsy enables the
pathologist to determine whether a malignant mass is invasive or in situ, whereas this determination
may not be possible on the basis of an FNA.
21. Does a normal-appearing mammogram in a woman with a palpable mass exclude
the possibility of cancer?
No. In general, the false-negative rate for mammograms is reported to be as high as 16%. Mammo-
grams can be interpreted as normal even in the presence of clinically evident cancer; for this reason,
any suspicious palpable mass should be examined by biopsy.
22. In what settings are mammograms particularly difficult to interpret?
Dense or very large breasts are difficult for radiologists to evaluate. This problem is found in 25% of
women and is particularly common at younger ages.
23. What is the role of ultrasound in the evaluation of solid breast masses?
Ultrasound is useful for differentiating solid from cystic masses. The study can be used in women with
large breasts who have deep, inaccessible lesions or who cannot undergo needle aspiration. It is also
preferred in pregnant and lactating women as the primary workup.
24. What is the approach to a woman whose mammogram shows a nonpalpable
lesion that is read as “probably benign” by the radiologists?
Two choices are possible: biopsy or repeat mammography within 6 months. Studies indicate that the
second approach is probably safe, but it depends on the comfort of the physician with the mammo-
graphic appearance and the patient’s ability to return for follow-up. The risk of malignancy in these
cases is less than 2%.
25. If a lesion is regarded as suspicious on a mammogram but is not palpable, what
is the next step?
Mammographic, ultrasound, or MRI localization techniques (including wires and dyes) can be used to
perform an image-guided biopsy.
26. What pathologic findings on breast biopsy put patients at a higher risk for subse-
quent development of breast cancer?
Lesions with a proliferative pattern are associated with an increased risk for subsequent cancer, and
lesions that show atypical hyperplasia have the highest relative risk (fivefold increase).
Table 19-1. Current Breast Cancer Screening Guidelines
ORGANIZATION MAMMOGRAM
CLINICAL BREAST
EXAMINATION
BREAST SELF-
EXAMINATION
American Cancer Society Age 40 years and
older annually
Age 20-39 every 1-3 years,
then annually ≥40 years
Optional for age 20
years and older
American College of
Obstetricians and
Gynecologists
Age 40 years and
older annually
Age 20-39 years every
1-3 years, then annually
≥40 years
Consider for high-risk
patients
U.S. Preventive Services
Task Force
Age 50-74 years
biennially
Insufficient evidence Not recommended
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27. What are the major types of breast cancer?
• Ductal: Most breast cancers involve ductal tissue. Ductal carcinoma is divided into infiltrating
ductal carcinoma and ductal carcinoma in situ (DCIS). DCIS identifies a woman at increased risk of
invasive breast cancer. Most women with DCIS develop infiltrating carcinoma, and a few women
have an invasive tumor present in the same breast at the time DCIS is diagnosed.
• Lobular: Approximately 10% of breast cancers are lobular. This category is subdivided into infiltrat-
ing lobular carcinoma and lobular carcinoma in situ (LCIS). LCIS is associated with an increased
risk of invasive breast cancer in either the ipsilateral or contralateral breast. Compared with DCIS,
the time to progression of LCIS is longer.
B
iBliography
1. American Cancer Society. Breast cancer early detection, 2014. Available at
http://www.cancer.org/acs/groups/cid/documents/webcontent/003165-pdf.pdf. Accessed November 18, 2014.
2. Dizon DS, Tejada-Berges T, Steinhoff MM, et al. Breast cancer. In: Barakat R, Markman M, Randall M, eds. Principles and
Practice of Gynecologic Oncology. 5th ed. Baltimore: Lippincott Williams & Wilkins; 2009:897–945.
3. Grube BJ, Giuliano AE. Benign breast disease. In: Berek J, ed. Berek and Novak’s Gynecology. 14th ed. Philadelphia:
Lippincott Williams & Wilkins; 2007.
4. National Comprehensive Cancer Network. Breast cancer risk reduction, 2014. Available at
http://www.nccn.org/professionals/physician_gls/pdf/breast_risk.pdf. Accessed November 18, 2014.
5. National Comprehensive Cancer Network. Breast cancer screening and diagnosis, 2014. Available at
http://www.nccn.org/professionals/physician_gls/pdf/breast-screening.pdf. Accessed November 18, 2014.
6. Pace L, Keating N. A systematic assessment of benefits and risks to guide breast cancer screening decisions. JAMA.
2014;311:1327–1335.
KEY POINTS: BREAST DISEASE
1. Breast pain occurs in more than two thirds of menstruating women; it tends to be diffuse, bilateral,
and cyclic.
2. Fibrocystic changes are the most common benign breast conditions. Such changes are character-
ized by fibrosis of breast stroma and the formation of cysts, and they typically affect women of
reproductive age.
3. The Gail model combines risk factors such as age, family history, personal history of breast biopsies,
age of menarche, and age of menopause to assess an individual’s breast cancer risk.
4. A palpable breast mass is initially evaluated with mammography or ultrasound, or both. FNA can
be done to assess whether the mass is cystic or solid; if bloody fluid or solid tissue is obtained, it
should be sent for cytologic examination. A core or excisional biopsy can enable a pathologist to
determine whether a malignant mass is invasive.
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1. What are the characteristics of intimate partner violence (IPV)?
IPV includes threatened or actual physical, sexual, or psychological abuse by a current or former
intimate partner. Most physical violence is accompanied by mental abuse and intimidation. IPV occurs
among individuals of all ages, ethnicities, and socioeconomic classes and within both heterosexual
and same-sex couples.
2. What is the incidence of IPV?
It is difficult to determine the true incidence because IPV is likely underreported, but 200 million cases
of IPV are estimated to occur in the United States annually. A female partner is the victim in approxi-
mately 90% of cases. In a survey conducted by the Centers for Disease Control and Prevention, 43.9%
of women and 23.4% of men experienced sexual violence, and 19.3% of women and 1.7% of men
reported a personal history of rape during their lifetime.
3. What are “red flags” that should heighten suspicion for IPV?
Multiple injuries with inconsistent explanations of how they occurred, frequent emergency
department or urgent care visits, missed appointments, significant difficulty with pelvic or rectal
examinations, and the presence of an overly attentive or verbally abusive partner at clinic visits.
The victim’s partner may be reluctant to leave the room during an examination or may even
refuse.
4. What somatic complaints and psychological conditions are associated with IPV?
Victims of IPV have a higher incidence of multiple physical complaints, including headaches,
chronic pain, insomnia, and irritable bowel syndrome. They also have a higher incidence of
depression, suicidality, anxiety, eating disorders, substance use and abuse, and posttraumatic
stress disorder.
5. Who should be screened for IPV?
• Any patient who presents with signs or symptoms suggestive of IPV
• Female trauma victims
• Female patients in the emergency department
• Women with chronic abdominal pain or chronic headaches
• Women diagnosed with sexually transmitted infections
All patients should be screened during an initial visit to a primary care provider or on presenta-
tion to a hospital, and pregnant women should be screened at their initial prenatal visit. Although
studies have demonstrated that routine screening of asymptomatic patients increases detection
of IPV, no studies have yet shown that screening improves health outcomes for the victim or the
perpetrator.
6. How should screening for IPV be performed?
It is important that patients feel safe and comfortable when asked questions about IPV. Partners and
family members should be asked to leave the room before questioning. Providers should ask open-
ended and direct questions while assuring confidentiality. Examples include the following:
• At any time, has a partner hit, kicked, or otherwise hurt or threatened you?
• I see patients in my practice who have been hurt or threatened by someone they love. Is this
happening to you?
7. What is the incidence of IPV during pregnancy?
Between 1% and 20%. A high rate of underreporting is suspected. Physical abuse during pregnancy
is frequently directed to the breasts and abdomen. Changes in violence patterns are variable during
pregnancy and the postpartum period, with one fifth of women reporting increased abuse and one
third reporting a decrease in abuse. Pregnant patients may feel additional pressure to stay in a rela-
tionship and conceal abuse.
CHAPTER 20
INTIMATE PARTNER VIOLENCE
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INTIMATE PARTNER VIOLENCE
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8. Are any pregnancy complications associated with IPV?
IPV has been associated with poor weight gain, infection, anemia, tobacco use, stillbirth, pelvic
fracture, placental abruption, fetal injury, preterm delivery, and low birth weight. The leading cause of
maternal mortality is homicide, and most cases are associated with a history of IPV.
9. What is a safety plan?
A safety or “exit” plan should be developed with a patient after she has divulged a history of IPV. This
plan can be implemented whenever a patient feels that violence is escalating and her life may be at
risk or at any other time she feels ready to leave her partner. A safety plan should include preparing
an emergency kit, identifying a safe place for her to go, and establishing a signal to alert children or
neighbors to call 911. Emergency kits should include important documents such as birth certificates
or passports, money, car keys, and necessary medications. If a patient does not have any nearby fam-
ily or friends, information about the nearest shelters should be provided.
10. What are the three phases of the cycle of domestic abuse?
The three phases are tension building, acute battering, and perpetrator apology and remorse. During
the tension building phase, tension between the couple escalates, and the victim may attempt to calm
or please the batterer in hopes of preventing abuse. In the acute battering phase, the victim sustains
verbal, sexual, or physical abuse. In the final phase, the batterer demonstrates remorse and may
apologize, make false promises, or even give the victim gifts. This cycle tends to repeat itself, with the
abuse often becoming more severe with time.
11. What resources should be provided to patients who are victims of IPV?
Providers should be aware of local resources such as community hotlines, shelters, support groups,
and social welfare services. Patients should be provided with telephone hotline numbers in a confi-
dential setting. Flyers in bathrooms or brochures in waiting or examination rooms are another way to
help patients access these resources, which include the following:
• National Domestic Violence Hotline: 1-800-799-7233 (1-800-799-SAFE)
• National Sexual Assault Hotline (1-800-656-4673)
BiBliography
1. Alpert EJ. Intimate Partner Violence: The Clinician’s Guide to Identification, Assessment, Intervention, and Prevention.
5th ed. Waltham, MA: Massachusetts Medical Society; 2010.
2. American College of Obstetricians and Gynecologists. Intimate partner violence. ACOG committee opinion no. 518.
Obstet Gynecol. 2012;119:412–417.
3. Breiding MJ, Smith SG, Basile KC, Walters ML, Chen J, Merrick MT. Prevalence and characteristics of sexual violence,
stalking, and intimate partner violence victimization: national intimate partner and sexual violence survey, United States,
2011;63. MMWR Surveill Sum; 2014:1–18.
4. Lentz GM. Rape, incest, and domestic violence. In: Katz VL, Lentz GM, Lobo RA, Gershenson DM, eds. Comprehensive
Gynecology. 5th ed. Philadelphia: Mosby; 2007:208–211.
5. McCloskey LA, Williams CM, Lichter E, Gerber M, Ganz ML, Sege R. Abused women disclose partner interference with
health care: an unrecognized form of battering. J Gen Intern Med. 2007;22:1067–1072.
6. Moyer VA. Screening for intimate partner violence and abuse of elderly and vulnerable adults: U.S. preventive services
task force recommendation statement. Ann Intern Med. 2013;158:478–486.
7. Nelson HD, Bougatsos C, Blanzina I. Screening women for intimate partner violence and elderly and vulnerable adults
for abuse: systematic review to update the 2004 U.S. Preventive Services Task Force Recommendation. Ann Intern Med.
2012;156:796–808.
KEY POINTS: INTIMATE PARTNER VIOLENCE
1. IPV includes threatened or actual physical, sexual, or psychological abuse by a current or former
intimate partner.
2. The cycle of abuse involves three phases: tension building, acute battering, and perpetrator apology
and remorse.
3. It is important that patients feel safe and comfortable when asked questions about IPV and that
confidentiality is assured.
3. Once a patient divulges a history of IPV, a safety plan should be developed, and she should be made
aware of local resources.
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1. What is the definition of puberty?
Puberty is the process by which the body undergoes hormonal changes and physical devel-
opment to reach full reproductive capacity. During this time, significant neuroendocrine and
physiologic changes in the reproductive system not only lead to the ability to ovulate and
menstruate in girls, but also cause accelerated linear skeletal growth and the development of
secondary sexual characteristics, including breast development and the appearance of pubic and
axillary hair.
2. What are the physical signs of puberty, and when do they occur and in what
order?
Puberty begins with an increase in linear growth velocity 1 to 2 years before the onset of breast
budding (thelarche) or the appearance of pubic and axillary hair (adrenarche). These changes are
followed by a period of maximum growth velocity (≈9 cm/year) and culminate in menarche.
• Mnemonic of order of puberty: GTAPM
• Growth spurt
• Thelarche
• Adrenarche
• Peak growth
• Menarche
The order of pubertal development varies based on race, as well as on individual characteristics.
Thelarche typically precedes adrenarche in white girls, but the opposite is true in African-American
girls. Approximately 10% of normal girls may experience menarche before adrenarche.
The age of puberty has decreased since the original descriptions published by Marshall and
Tanner in 1969. The Pediatric Research in Office Settings (PROS) study in 1997 provided more con-
temporary data, showing that the mean ages for thelarche, adrenarche, and menarche were 8.9, 8.8,
and 12.2 years for African-American girls and 10, 10.5, and 12.8 years for white girls.
3. What is Tanner staging?
In 1969, Dr. J.M. Tanner developed a system to grade the normal development of puberty by compar-
ing breast and pubic hair development in girls (Table 21-1 and Fig. 21-1) and genital and pubic hair
development in boys.
4. What are the hormonal changes that occur with puberty?
Puberty and the menstrual cycle depend on a normally functioning hypothalamic-pituitary-ovarian
(HPO) axis.
The first neuroendocrine change to occur in puberty is an increase in the amplitude of
gonadotropin-releasing hormone (GnRH) pulses from the hypothalamus as it becomes less sensitive
to negative feedback from low levels of estrogen. This change triggers an increase in luteinizing hor-
mone (LH) release from the pituitary beginning at night, with a lesser increase in follicle-stimulating
hormone (FSH) pulses.
These pulses stimulate the growing ovarian follicles to release estradiol, which ultimately initi-
ates an LH surge capable of triggering ovulation. Progesterone is released from the corpus luteum
following ovulation (in the luteal phase of the cycle).
During this time (≈6 to 8 years of age), the adrenal gland is also starting to produce increased
levels of androgens independent of the HPO axis, which leads to adrenarche.
5. What factors determine when puberty starts?
Family history, race, geographic factors, and body composition all play roles in the timing of initiation
of puberty. A family history of early puberty, African-American race, and living closer to the equator, at
lower altitude, and in urban settings predispose to early puberty. Adipose tissue contains the enzyme
CHAPTER 21
PUBERTY
Michelle S. Özcan, MD, and Travis W. McCoy, MD
II REPRODUCTIVE ENDOCRINOLOGY
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aromatase, which catalyzes the conversion of testosterone to estradiol, thus increasing the likelihood
of early puberty in obese women. Conversely, Frisch and Revelle proposed that a critical body fat
content of 17% to 22% is necessary to initiate puberty; girls with anorexia nervosa, poor nutrition,
excessive stress, or excessive exercise may suppress their HPO axis and experience delayed puberty
or amenorrhea.
6. What are the age limits for the normal onset of puberty?
The generally accepted range for the onset of puberty is between 8 and 14 years. The Pediatric
Research in Office Settings (PROS) study in 1997 showed that approximately 50% of African-American
girls had initiated puberty by age 8 years, and 40% of white girls had initiated puberty by age 9 years.
Based on these results, revised guidelines recommend that puberty be considered precocious when
thelarche or adrenarche begins before age 6 years in African-American girls or age 7 years in white
girls. Girls who do not have any secondary sexual characteristics by age 13 years or no menses by
15 years of age with normal development of secondary sexual characteristics are considered to have
delayed puberty.
Table 21-1. Classification of Female Breast and Pubic Hair Development
CLASSIFICATION DESCRIPTION
Breast Growth
B1 Prepubertal: elevation of papilla only
B2 Breast budding
B3 Enlargement of breasts with glandular tissue, without separation of
breast contours
B4 Secondary mound formed by areola
B5 Single contour of breast and areola
Pubic Hair Growth
PH1 Prepubertal: no pubic hair
PH2 Labial hair present
PH3 Labial hair spreading over mons pubis
PH4 Slight lateral spread
PH5 Further lateral spread to form inverse triangle and reach medial thighs
Modified from Roy S. Puberty. In: Mishell DR Jr, Davajan V, eds. Infertility, Contraception, and Reproductive
Endocrinology. 4th ed. Malden, MA: Blackwell Scientific; 1997:225-226.
Figure 21-1. Pubertal staging according to Tanner stage. (From Ross GT, Vande Wiele R. The ovary. In: Williams RH, ed.
Textbook of Endocrinology. 5th ed. Philadelphia: Saunders; 1974. As redrawn in Rosenfeld RL, Cooke DW, Radovick S.
Puberty and its disorders in the female. In: Sperling MA, ed. Pediatric Endocrinology. 4th ed. Philadelphia: Saunders; 2014.)
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7. Which patients should be evaluated for precocious puberty and for delayed puberty?
• Precocious puberty
• All girls younger than 6 years of age with breast or pubic hair development
• Girls younger than 8 years of age with both breast and pubic hair development
• Girls younger than 8 years of age with only breast or pubic hair development: careful history and
examination with a bone age determination and close follow-up
• Delayed puberty
• No breast development by age 13 years
• Absence of menarche by age 15 years
• Absence of menarche within 3 years of thelarche
• Absence of menarche by age 14 years if hirsutism is present or there is concern for an eating
disorder, excessive exercise, or outflow tract obstruction
8. Is precocious puberty more common in girls or boys, and what about delayed
puberty?
Precocious puberty is up to 23 times more common in girls, but delayed puberty is more common in
boys. Girls progress faster through puberty than boys by completing puberty in an average of 3 years
as opposed to 5 years for boys. The incidence of precocious puberty in girls in the United States is
approximately 1 in 10,000.
9. What are the classes of precocious puberty?
• GnRH-dependent (central): caused by early activation of the HPO axis. Pulsatile GnRH release
triggers LH and FSH release, which leads to gonadal sex steroid production. Puberty begins earlier,
but it usually proceeds at the normal pace.
• GnRH-independent (peripheral): resulting from excess sex steroid exposure independent of hypo-
thalamic GnRH release. This exposure can originate from the gonads, adrenals, or from exogenous
administration.
10. What is the difference between GnRH-dependent and GnRH-independent
precocious puberty?
GnRH-dependent (“central” or “true”) precocious puberty is characterized by early activation of the
HPO axis. This leads to breast and pubic hair development in girls and to pubic hair development and
testicular enlargement in boys. The puberty is characterized as “isosexual,” meaning that the changes
are consistent with the child’s sex.
GnRH-independent (“peripheral” or “pseudo”) precocious puberty refers to pubertal changes that
are independent of the HPO axis; instead, they are the result of exposure to hormones that derive from
the gonads, the adrenals, or the environment. Exposure to external hormones can sometimes cause
activation of the HPO axis and lead to a mixed picture. This type of precocious puberty can be “iso-
sexual” or “contrasexual,” meaning that the changes are inconsistent with the child’s sex—virilization
in girls exposed to androgens (e.g., acne, hirsutism, clitoromegaly, voice deepening) or feminization in
boys exposed to estrogens.
11. What is incomplete precocious puberty?
Incomplete precocious puberty refers to isolated premature thelarche or adrenarche with a normal
bone age and laboratory values. Usually, it simply represents a variant of normal pubertal develop-
ment. These changes still require evaluation and close follow-up at a minimum, however, because
they may sometimes progress to complete precocious puberty.
12. What are the causes of GnRH-dependent precocious puberty, and how are they
treated?
Up to 90% of cases of GnRH-dependent precocious puberty are idiopathic. Idiopathic GnRH-depen-
dent precocious puberty is treated when bone age is advanced by 1 year or more, when growth
velocity is greater than 6 cm/year, or when predicted adult height is lower than the target range.
Treatment is with long-acting GnRH agonists such as leuprolide acetate, which causes pituitary
desensitization and downregulation of receptors leading to a decrease in gonadotropin release and
subsequent hypogonadism. Breast development should cease, and growth velocity and the pace of
advancing bone age should decrease. The patient should be monitored every 3 to 6 months, and
treatment should be stopped when epiphyses fuse or pubertal and chronologic ages are appropriately
matched.
Cerebral disorders account for 7% to 10% of cases of GnRH-dependent precocious puberty.
These disorders can result from congenital malformations (hamartomas), tumors, hydrocephalus,
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