“Approved”
on methodological meeting
of Department of Obstetrics and Gynecology
with course of Infant and Adolescent Gynecology
“___”______________________ 201_ year
protocol #
T.a. The Head of the department
Professor
________________ O. Andriyets
METHODOLOGICAL INSTRUCTION
for practical lesson
“Reproductive disorders in infants and adolescents”
MODULE 4: Obstetrics and gynecology
CONTEXT MODULE 12 GYNECOLOGY DISEASES:
Subject: Obstetrics and Gynecology
6th year of studying
2nd medical faculty
Number of academic hours – 6
Methodological instruction developed by:
ass.prof. Andriy Berbets
Chernivtsi – 2010
I. Topic: Abnormalities of sexual development of girls. Classification, clinical picture,
diagnostics and principles of treatment
II. Class duration – 4 hours.
III. Educational objectives:
The student must know:
1. Special methods of examination in girls with abnormalities of sexual development.
2. Deontology of communication with patients with such pathology in juvenile age.
3. Estimate data of general clinical, special, hormonal, roentgenological, medical and
genetic examination of girls with abnormalities of sexual development.
The student must be able to:
 Examine of a patient with abnormalities of sexual development.
 Make diagnostics and treatment.
 Interpret data of clinical and laboratorial and instrumental examination.
IV. Advice to the student.
Disorders of Puberty

Delayed Puberty
o Delay of puberty can be caused by anatomic abnormalities, chromosomal
disorders, neoplastic growths, or nutritional deficiencies.
o Commonly presents as a physical delay in maturation combined with amenorrhea.
o Causes of delayed puberty can be classified, based on the level of follicle
stimulating hormone (FSH) present, as outlined in Table 30.5.
o Hypergonadotropic Hypogonadism (High FSH)
A sufficient amount of gonadotropins are present, but the end organs are not
responsive and therefore do not produce sex steroids.



Gonadal dysgenesis
Present as phenotypic female with persistent prepubertal
development. Usually lack breast development.
May have some secondary sex characteristics and spontaneous
menstruation. Most often associated with primary amenorrhea.
Table 30.5 An
Differential Diagnosi Review of Causes of Delayed Puberty

Gonadal dysgenesis syndromes: Turner's syndrome, Sweyer's
syndrome

Primary ovarian failure






Constitutional delay
Intracranial neoplasms
Isolated gonadotropin deficiencies
Hormone deficiencies
Kallmann syndrome
Prader-Labhart-Willi syndrome


Laurence-Moon-Biedl syndrome
Chronic disease and malnutrition
Anatomic deformities Result in normal development with primary amenorrhea.



Imperforate hymen
Transverse vaginal septum
MГјllerian agenesis

o
Turner syndrome (45, X) is most commonly associated with
gonadal dysgenesis. Occurs in 1 in 2,000 to 2,500 born girls and is
present in approximately 6% of all spontaneous abortions (3).
 Sweyer syndrome(46, XY) is also associated with gonadal
dysgenesis, but patients often have a normal-to-tall stature. Most
often related to a mutation or structural abnormality of the Y
chromosome. Must remove gonads.
 Primary ovarian failure
 Ovaries develop but do not contain oocytes; may be associated
with chemotherapy, radiation, galactosemia, gonadotropin
resistance, autoimmune ovarian failure, or ovarian failure
secondary to previous infection.
 Treatment involves administration of exogenous estrogen and
progesterone to avoid osteoporosis and to facilitate development of
secondary sexual characteristics.
Hypogonadotrophic Hypogonadism (Low FSH)
An insufficient level of gonadotropins is present to permit follicular development
and therefore sex steroids are not produced.





Chronic disease of malnutrition: Conditions including states of
malnutrition, including starvation, anorexia nervosa, cystic fibrosis,
Crohn's disease, diabetes mellitus, inflammatory disease, and
hypothyroidism, are thought to lead to a disruption of gonadotropinreleasing hormone GnRH production, therefore resulting in pubertal delay
(4).
Constitutional delay: A delay in the (GnRH) pulse generator postpones the
normal physiologic events of puberty.
Intracranial neoplasms: Both craniopharyngiomas and pituitary adenomas
may cause delayed puberty. Visual symptoms are often associated with
these tumors, as is short stature and diabetes insipidus. Diagnosis is by CT
or MRI of the head. Treatment includes either surgical excision or
radiotherapy.
Isolated gonadotropin deficiencies: often secondary to abnormalities in
genes encoding proteins related to GnRH, FSH, or leutinizing hormone
(LH) (3).
Hormone deficiencies: Any aberration of growth hormone or thyroid
hormone levels will affect puberty. Therefore, these levels should be
investigated and treated appropriately. In addition, hyperprolactinemia can
cause a decrease in levels of FSH and LH and thus delay puberty.

o
Kallmann syndrome: A sporadic or X-linked syndrome with a classic triad
of anosmia, hypogonadism, and color blindness. The hypothalamus cannot
secrete GnRH due to dysfunction in the arcuate nucleus. Few or no
secondary sexual characteristics are present.
 Prader-Labhart-Willi syndrome: an autosomal dominant condition
associated with extreme obesity, emotional instability, and delayed
puberty secondary to hypothalamic dysfunction (4).
 Laurence-Moon syndrome: a rare autosomal disorder associated with
retinitis pigmentosa, hypogonadism, and spastic paraplegia (4).
 Bardet-Biedl syndrome: a rare autosomal recessive disorder associated
with retinitis pigmentosa, hypogonadism, and postaxial polydactyly (4).
Eugonadism (Normal FSH)
In cases of eugonadism, the hypothalamic-pituitary-gonadal axis remains intact,
and delay of puberty presents with primary amenorrhea related to anatomic
abnormalities in the genitourinary tract, androgen insensitivity, or inappropriate
positive feedback mechanisms.



Anatomic abnormalities of the genitourinary tract resulting in primary
amenorrhea:
 Imperforate hymen: may be evident in a neonate and may regress
as the girl enters childhood. After menarche, the imperforate
hymen may become evident when accumulating menstrual blood
forms a hematocolpos and may present as an abdominal mass.
Surgical intervention is required to incise the hymen and allow
stored debris to escape.
 Transverse vaginal septum: due to failure of canalization of
mГјllerian tubules and the sinovaginal bulb, leaving a membrane
present. May be associated with urinary tract abnormalities as well.
If the membrane is thin, it can be incised and dilated. If it is thick,
surgical excision with a split thickness skin graft may be required.
 MГјllerian agenesis: failure of the mГјllerian tract to develop
results in a blind vaginal pouch without uterus or fallopian tubes
present. Ovaries are present and function normally and, therefore,
puberty progresses as usual with primary amenorrhea as a
presenting complaint. This must be distinguished from androgen
insensitivity, as described later. One-third of these patients have
associated urinary tract anomalies, and 12% have skeletal
anomalies. A neovagina can be created by progressive dilation or
surgery.
 Vaginal atresia: The lower vagina is replaced by fibrous tissue;
differentiated from mГјllerian agenesis by the presence of normal
uterus and fallopian tubes.
Androgen insensitivity: discussed later under male feminization.
Karyotype XY males present as phenotypic females with a blind vaginal
pouch secondary to an insensitivity of circulating androgens.
Other causes of primary amenorrhea with eugonadism include
anovulation, androgen producing adrenal disease, and polycystic ovarian
syndrome.

Precocious Puberty
o Precocious puberty is a rare condition that occurs in only 1 of 10,000 girls (5).
o Defined as evidence of secondary sexual characteristics, including breast or pubic
hair development at an age more than 2.5 standard deviations below the mean (5).
o According to a recent study, such findings should be investigated in African
American girls under age 6 and Caucasian girls under age 7 (6).
o Characteristic accelerated growth velocity in combination with rapid bone growth
and maturation can result in short adult stature (7).
o Common causes of precocious puberty can be divided into GnRH-dependent
disorders, or true or central precocious puberty, versus GnRH-independent
disorders, or pseudoprecocious puberty.
o Central Precocious Puberty
 Most commonly idiopathic; secondary sexual characteristics progress in
normal sequence but more rapidly than in normal puberty, and may
fluctuate between progression and regression.
 Related to premature development of the hypothalamic-pituitary axis and
is therefore GnRH-dependent, but the initiating cause is unknown (5).
 May be transmitted in an autosomal recessive fashion, so check family
history.
 Often ovarian follicular cysts are present due to elevated levels of LH and
FSH (5).
 Other causes of central precocious puberty involve central nervous system
disease:
 Disease often involves areas surrounding the hypothalamus; mass
effect, radiation, or ectopic GnRH secreting cells are thought to
cause premature activation of pulsatile secretion of GnRH from the
hypothalamus.
 Diagnosis by CT or MRI of the head; history may be significant
for headache, mental status changes, mental retardation,
dysmorphic syndromes, along with the premature development of
secondary sexual characteristics.
 Treatment should be directed at the underlying cause; the location
of many of such tumors makes resection difficult, and, as a result,
chemotherapy or radiation may be involved.
 GnRH agonist administration can result in a short burst of gonadotropin
release followed by down-regulation and desensitization resulting in an
overall decrease in the level of circulating gonadotropins. Follow estradiol
levels to make appropriate dose adjustments (8).
o Pseudoprecocious Puberty
 Premature development of secondary sexual characteristics occurs by a
GnRH-independent mechanism.
 Differential diagnosis includes estrogen-secreting tumors, benign
follicular ovarian cysts, McCune-Albright syndrome, Peutz-Jeghers
syndrome, adrenal disorders, and primary hypothyroidism.
 Estrogen secreting ovarian tumors
 Granulosa cell tumors (60%): usually >8 cm in size; 80% are
palpable
on
abdominal
examination;
others
include
arrhenoblastomas, thecomas, lipid cell tumors, teratomas, or
choriocarcinomas.
 Diagnose by sonography, manage surgically with adjuvant
chemotherapy, if indicated, and follow by estradiol levels.
 Benign follicular ovarian cysts



Most common form of estrogen-secreting masses in children
May require a diagnostic laparoscopy versus exploratory
laparotomy to differentiate from a malignant tumor. Removal of
the cyst may be therapeutic.
 McCune-Albright syndrome
 Triad: cafГ© au lait spots, polyostotic fibrous dysplasia, and cysts
of skull and long bones; precocious puberty is present in 40% (9).
 Sexual precocity results from recurrent follicular cyst. Removal of
cyst is not helpful.
 Aromatase inhibitors (i.e., testolactone) may help symptoms.
 Evaluate with serial pelvic sonograms to detect the presence of
gonadal tumors.
 Peutz-Jeghers syndrome
 Commonly characterized by mucocutaneous pigmentation and GI
polyposis
 Also associated with rare sex cord tumors, including epithelial
tumors of the ovary, dysgerminomas, or Sertoli-Leydig cell
tumors, whose estrogen secretion may result in feminization and
incomplete sexual precocity
 Girls with Peutz-Jeghers syndrome should be screened with serial
pelvic sonograms.
 Adrenal disorders
 Some adrenal adenomas have been noted to secrete estrogen alone
and may therefore give rise to sexual precocity.
 Primary hypothyroidism
 Characterized by premature breast development and galactorrhea
without an associated growth spurt
 Key points in evaluation and management of precocious puberty
 Perform a detailed evaluation with Tanner staging.
 Laboratory data should include LH, FSH, estradiol, progesterone,
17-hydroxyprogesterone, DHEA, DHEAS, TSH, T4, hCG (5).
 A GnRH stimulation test would provide a definitive diagnosis of
central precocious puberty (5).
 Obtain an x-ray to determine bone age. Head CT or MRI can rule
out an intracranial mass. Abdominal/pelvic ultrasound can be used
to evaluate the ovaries (5).
 Goals for management include maximizing adult height and
delaying maturation until a normal age of puberty. Treat the
intracranial, ovarian, or adrenal pathology if present and attempt to
reduce associated emotional problems (8).
Male Feminization
o Genetic males (XY) undergo feminization related to androgen insensitivity.
o Complete androgen insensitivity, or “testicular feminization” (10).
 Transmitted in a maternal X-linked recessive fashion
 Pathophysiology: Androgen presence is unable to induce the Wolffian
duct to mature and, as a result, seminal vesicles, vas deferens, and
epididymis do not form. AntimГјllerian hormone is present so mГјllerian
duct formation remains inhibited such that uterus, cervix, and fallopian
tubes do not form either. The resulting phenotype is female, with a vagina
derived from the urogenital sinus that ends in a blind pouch, and testes
that often descend through the inguinal canal.


Clinical presentation: primary amenorrhea, Tanner stage V breast
development, scant axillary and pubic hair
 Management: gonadectomy is recommended secondary to an increased
incidence of malignancy; exogenous estrogen therapy is also
recommended.
o Incomplete androgen insensitivity (10)
 Less common with presentation ranging from near complete
masculinization to near complete failure or virilization.
 As minimal sensitivity to androgens is present, the Wolffian duct system
develops to some extent, although spermatogenesis usually remains
absent.
 Physical exam may include a range of clitoromegaly or ambiguous
genitalia.
 Sex assignment depends on the degree of masculinization present; if a
male sex assignment is made, caution should be taken because
gynecomastia may occur during puberty, if androgen receptor presence is
inadequate.
o 5-alpha reductase deficiency is a condition in genotypic males (XY) who are
phenotypically female in the prepubertal state and become phenotypic men at
puberty. No breast development is present, which distinguishes this condition
from androgen insensitivity. Normal testicular function is present.
Female Virilization
o Genetic females (XX) are exposed to increased androgen levels that lead to
inappropriate virilization, most often an indicator of organic disease in girls.
o Virilizing congenital adrenal hyperplasia (CAH): most commonly associated with
deficiency of 21-hydroxylase, an autosomal recessive disorder. Many present as
the newborn girl with ambiguous genitalia and possible associated salt-wasting
due to mineralocorticoid deficiency. Virilization may also be delayed until later
childhood, related to androgen excess at that time (11).
o Cushing's disease: may result from an adrenal carcinoma and may manifest as
growth failure, with or without virilization, obesity, striae, or moon facies.
o Ovarian tumors: arrhenoblastoma is the most common virilizing ovarian tumor.
Others include lipoid cell tumor and gonadoblastoma.
VIII. Premature Thelarche




Definition: bilateral breast development without other signs of sexual maturation in girls
before age 8 (12).
Commonly occurs by age 2 and is rare after age 4.
The etiology behind premature thelarche is unclear, but an exogenous estrogen source
must be excluded. Not known to be associated with central nervous system pathology and
is not known to be a familial condition. The mechanism is thought to be related to a
temporary activation of the hypothalamic-pituitary-gonadal axis with increased FSH
secretion (12).
Upon finding during physical examination, precocious puberty must be ruled out:
o Document the appearance of the vaginal mucosa, breast size, and presence or
absence of a pelvic mass on pelvic/rectal examination.
o Determine bone age with radiographic imaging; should be within normal range in
premature thelarche and advanced in precocious puberty.
o Pelvic sonography should demonstrate a normal prepubertal uterus.
o


Plasma estrogen levels may be mildly elevated, but dramatic elevations suggest
another etiology. Stimulated responses of LH and FSH may be obtained and are
both generally elevated in precocious puberty, whereas only stimulated FSH is
elevated in premature thelarche (12).
Also, review recently used medications and topical creams as application of topical
conjugated estrogens (Premarin) for longer than 2 to 3 weeks, which may result in breast
changes.
Prognosis: In idiopathic cases, a regression in breast enlargement often occurs after a few
months but may persist for several years. In approximately 50% of patients, breast
development can last 3 to 5 years.
Physical Examination and Evaluation for Sexually Transmitted Infections
The exam of a potentially sexually abused child should include a general exam. Attention
should be directed at evaluating skin for bruising, lacerations, or trauma. Parents or
concerned adults should be counseled that a genital exam in children who have been abused
is usually normal. Physical evidence is present in less than 5% of children. The genital exam
should be carried out as described earlier in this chapter.
In situations in which abuse has occurred within 72 hours careful collection of forensic
evidence is important. Collection of all clothing and undergarments is critical. Motile sperm
will be present in the prepubertal vagina for approximately 8 hours, and nonmotile sperm for
approximately 24 hours. Since prepubertal children do not have cervical mucous, sperm do
not exist for the longer durations seen in reproductive females within the cervical canal.
“Rape” kits will also often include testing for a protein specific to the prostate. Vaginal
specimens may be obtained by using small swabs within the vagina, similar to the method
described for obtaining vaginal cultures.
Given that only approximately 5% of abused children acquire a STI (sexually transmitted
infection), providers must decide when STI testing is indicated. Both gonorrhea and
chlamydia cause a vaginitis not a cervicitis in prepubertal children, so a vaginal culture
should be done. In the United States a vaginal culture for gonorrhea and chlamydia, not DNA
testing should be performed as recommended by the Centers for Disease Control and
Prevention. Since nonculture methods are not labeled for use in children, positive testing may
not be admissible in court. Testing in prepubertal children is also influenced by typical
incubation intervals of STIs. If a child was abused in an isolated incident, an STI may not be
found on testing immediately after the abuse.
In children presenting in nonacute presentations the pro-vider must decide whether to
perform testing for STIs. It is very rare for a child to have gonorrhea or chlamydia without a
vaginal discharge. Standards of care regarding this issue may differ in various locations.
Hymens in the Evaluation of Sexual Abuse
There is a general misunderstanding regarding the significance of hymeneal changes. The
transverse diameter of the hymen was previously used as a marker of abuse. However, it is
now clear that there is significant variation in children, and the state of the hymen it is not a
reliable marker of abuse. Complete transections of the hymen and clefts that extend to the
junction of the hymen between 3 o'clock and 9 o'clock are not congenital, but if present could
be from abuse or a child inserting an object. Controversies exist as to the significance of
incomplete transections
Genital Warts
Human papillomavirus (HPV) the causative agent of genital warts may be transmitted to
children from the maternal genital tract at delivery or by sexual or nonsexual transmission
after birth. The incubation interval from transmission to the pres-ence of visible genital warts
has not been defined in children; however, it appears likely that most warts appearing prior to
approximately 2 years of age are from maternal–child transmission. If the child is 2 years of
age or older, serious consideration should be given to the possibility of sexual transmission.
(See previous section on sexual abuse in this chapter). However, genital warts “discovered”
in a 3-year-old may have been present for some time prior to being noticed. This is
particularly a problem in the perianal area, which may not be examined carefully even in
children undergoing a cursory genital exam as part of well-child annual care.
Approximately half of lesions will regress over 5 years. Expectant management is
reasonable, but parents may prefer treatment. Treatment in children is difficult. Caustic
treatments such as trichloroacetic acid are painful even if children are pretreated with local
anesthesia. Topical imiquimod cream is labeled for use in children 12 years and older. If
imiquimod cream is acci-dentally carried by the child to the cornea it could cause damage to
the eye. Laser treatment is an option for significant wart tissue, but must be performed under
an inhalation anesthesia and can be associated with significant postoperative pain.
VULVITIS
The skin covering the vulva may be involved in any generalized dermatological disorder but
its special anatomical situation makes it liable to a number of inflammatory conditions which
are confined to the genital area. Although microorganisms abound in the vulval and perineal
regions, normal skin is resistant to invasion by most of these. However, if the skin is
continually moist because of vaginal discharge or urinary incontinence, irritation may occur.
This leads to scratching, damage to the macerated skin and a reduction in resistance to
infection. Resistance of the skin to infection is also reduced if there are atrophic or
degenerative changes as a result of disease or reduced oestrogen levels after the menopause.
Specific organisms may also cause infection; for example, staphylococci may infect
sebaceous glands or hair follicles, Candida albicans may grow freely if there is glycosuria
and treponemata or other organisms may be transmitted at coitus.
In addition, non-infective dermatitis may be caused by sensitivity reactions to chemical
agents such as medicinal applications, the detergents used for washing underclothes, or toilet
preparations.
Because there are so many causes of vulvitis, careful investigation is always necessary. A
full gynaecological history and examination are required. Special attention must be paid to
any skin disorders elsewhere. The urine must be tested for sugar and examined
bacteriologically. Any vaginal discharge must be investigated. On occasion rectal swabs
should be examined and proctoscopy may be required. The skin may be examined bacteriologically and by histological examination of scrap-ings or a biopsy.
Although vulvitis may be acute or chronic an aetiological classification is more satisfactory:
vulvitis due to specific infections vulvitis due to sensitivity reactions vulvitis secondary to
vaginal discharge or urinary disorders vulval dystrophies. As these conditions are not strictly
inflammatory they are considered in a separate section.
VULVITIS DUE TO SPECIFIC INFECTIONS
Gonorrhoea
Gonococci do not invade the vulval skin, but may cause infection of Skene's tubules at the
lower end of the urethra. They may also cause a Bartholin's abscess, although this lesion is
more commonly due to other organisms.
Syphilis
The vulva may be affected by a primary chancre. In the secondary stage condylomata lata
appear as raised plaques with a slightly indented top covered by a greyish exudate.
Lymphogranuloma venereum This chronic sexually transmitted disease is caused by a strain
of Chlamydia trachomatis.
Granuloma inguinale
This is another sexually transmitted disease of tropical origin. The organism causing it is
uncertain.
Tuberculosis
Vulval tuberculosis is very rare. Infection is secondary to other lesions higher in the genital
tract. An ulcer is formed with bluish undermined edges.
Furunculosis
Staphylococci may infect the hair follicles on the outer aspect of the labia majora.
Bacteriological examination of the pus will decide the choice of an antibiotic.
Fungal infections
Candidiasis
In diabetic patients with glycosuria, vulvitis due to infection with Candida albicans may
occur. The whole vulva is inflamed, with an appearance described as being that of red beef.
The urine should be tested for sugar in all cases of vulvitis. However, infection with Candida
is not confined to diabetics, and is common during pregnancy especially if the renal threshold
for sugar is lowered. It may also occur in patients who are using oral contraceptives or who
have recently been given antibiotics. The use of tight-fitting nylon underwear, which
prevents normal skin aeration, encourages recurrent infection. The vagina is often the primary site of infection and the fungus is usually easily found there, but it can also be
demonstrated by staining scrapings of the vulval skin.
Treatment of diabetes, if that is present, will often clear up the infection. Vulval infection
will usually resolve if the vaginal infection is treated with fungicidal pessaries or creams. In
resistant cases, an alternative treatment is to paint the vagina and vulva with an aqueous
solution of gentian violet (0.5 per cent). The dye will stain clothing, and the patient should be
warned of this.
Parasitic infections
Enterobius vermicularis
Threadworms from the anus may cause vulval irritation in children. The worms are easily
seen in the stools, and the irritation is relieved when they are eradicated from the bowel.
VULVITIS DUE TO SENSITIVITY REACTIONS
The vulval skin may become sensitized to many agents, with resulting dermatitis. These
agents include detergents, deodorants, dusting powders, local anaesthetics and ointments
prescribed by a doctor or bought by the patient from a chemist for the relief of pruritus.
Sensitivity to contraceptive creams, to the rubber of contraceptive caps or condoms, or to
powder used with them may also occur.
In any case of vulvitis careful enquiry must be made about any local applications to the
vulval area and any recent changes in the use of toilet preparations or contraceptives. Patch
tests can sometimes identify the offending agent. Any substance under suspicion must be
withdrawn and zinc or calamine cream applied
VULVITIS SECONDARY TO VAGINAL DISCHARGE OR URINARY DISORDERS
Vulvitis may be secondary to vaginitis, for example, in cases of profuse discharge due to
infection with Trichomonas vaginalis. Irritation will occur if there is sufficient vaginal
discharge from any cause to keep the vulval skin continually moist, and scratching will add
to the damage to the skin. If there is urinary incontinence, especially if the urine is also
infected, vulvitis may ensue; the association with glycosuria has already been mentioned. In
vulval dermatitis of long standing there may be some thickening and pigmentation of the
skin, but the skin soon recovers when the cause is removed.
BARTHOLINITIS
The vestibular gland of Bartholin lies on each side of the vulva beneath the posterior third of
the labium minus; its duct opens into the posterior part of the vestibule. The gland may be
infected by gonococci, staphylococci, streptococci or with a mixture of organisms, including
Escherichia coll. The result is an abscess which forms a painful red swelling and expands the
posterior part of the labium minus. It causes severe discomfort when walking or sitting.
In the very early stages it may be possible to abort the infection with an antibiotic such as
ampicillin, but patients almost always present too late for this. The treatment is then to drain
the abscess. This is best done by marsupialization; an elliptical piece of skin and the
underlying anterior wall of the abscess are excised. The remaining abscess wall and skin
edge are sutured with interrupted plain catgut sutures around the perimeter to prevent
reformation. The pus is cultured so that the appropriate antibiotic can be chosen.
Bartholin's cyst
The duct of the gland may become blocked. It then becomes distended with the mucoid
secretion of the gland and forms a cyst, which lies beneath and expands the posterior part of
the labium minus. Such a cyst may become infected, but otherwise it is painless. If the cyst
interferes with comfort at sexual intercourse, the cyst is marsupialized as described above. In
a few days the wide opening contracts down. This simple procedure is much easier and more
effective than excising the cyst and gland from the vascular field in which they lie.
VAGINAL DISCHARGE
Changes in the activity of the vaginal epithelium and in the vaginal secretion which occur at
different times during a woman's life have a profound influence on the defence against
vaginal infection.
In the adult the normal vaginal moisture or secretion consists of vaginal transudate
containing desquamated vaginal epithelial cells, which may give it a creamy colour, mucus
secreted by the cervical glands and, to a small extent, secretion from the endometrial glands.
Its viscosity depends mainly on the cervical component.
There is a cyclical variation in the amount of secretion; it is heavier premenstrually and there
is an increased secretion of clear cervical mucus at the time of ovulation. There are no glands
in the vagina and the transudate passes through the stratified epithelium. The epithelium
contains glycogen, which is converted to lactic acid by Doderlein's bacilli, which are
normally present in the vagina. As a result, the vaginal fluid is acid (pH 4-5) and this
prevents the multiplication of most pathogenic organisms.
Vaginal discharge is a very common gynaecological symptom. Its significance is sometimes
difficult to assess, and the complaint is occasionally the patient's way of expressing anxiety
about matters about which she feels less free to talk— sexual problems or fear of cancer, for
example. Discharge may be of varying significance in different cases; an increase which
causes complaint in one woman may be less than that which others call normal; the change in
amount is the significant point. Vaginal discharge seldom has a noticeable odour unless it is
associated with anaerobic organisms; these occur often with foreign bodies, such as tampons
and necrotic tissue as found in retained products of conception and carcinoma. In the past a
complaint from the patient that everybody could smell the discharge was attributed to
psychological overlay, but nowadays such a musky discharge is often recognised as a
Gardnerella vaginalis infection.
Assessment of the amount of discharge can be difficult. Persistent moistness, a stain on the
underclothes or the need to wear a pad give a rough guide when related to an estimate of the
patient's normal standard of hygiene.
There is a natural increase in the vaginal moisture or secretion at the time of ovulation,
premenstrually and during pregnancy. The contraceptive pill may cause an increase in
cervical secretion and so may a cervical erosion. The term leucorrhoea, which is now used
frequently, should be confined to an increase in the physiological secretion.
When infection supervenes, the clear or white secretion becomes purulent and coloured and
large numbers of leucocytes appear in the vaginal cavity, presumably entering by diapedesis
through the vaginal wall. In children and postmenopausal women oestrogen levels are low
and, although at these ages the vagina may be less exposed to infection, vaginitis may still
occur because of the loss of the acid barrier.
Vaginitis is one of the most common gynaecological complaints; the primary symptom being
discharge. About 90 per cent of patients with vaginitis suffer from infection of the vagina
caused by Candida, Gardnerella or Trichomonas. In addition to the discharge there is often a
presenting complaint of vulval irritation and itching, which may lead to scratching. On
examination the vaginal mucosa will often appear erythematous and congested, and in the
majority of cases an infected vaginal discharge, often showing characteristic diagnostic
features of a specific infection, will be present.
INFECTIVE VAGINITIS AND VAGINAL DISCHARGE
MONILIAL VAGINITIS
This is a fungal infection with Candida albicans and is especially likely to occur in patients
who have glycosuria; the urine must be examined for sugar in every case in which this
infection is found. Apart from cases of diabetes, infection may occur during pregnancy when
the renal threshold for
glucose may be low. Infection may also occur in patients who are using oral contraceptives
or are being treated with antibiotics for some other condition. The infection maybe
transmitted sexually.
There is intense vulval irritation and accompanying vaginal discharge. There is sometimes
redness and inflammation of the vulval skin, which may spread to the thighs. Examination
may be difficult because of tenderness. With heavy infection the discharge is thick and white
and when it is removed the vaginal wall is seen to be red and inflamed. Not every case shows
the typical white discharge, and diagnosis must not depend on naked-eye appearances alone
because the fungus can be demonstrated in the clinic in wet preparations when mycelial
threads are seen. The organism grows easily in laboratory cultures in which Gram-positive
mycelia and spores are seen.
Treatment
Fungicides are usually inserted into the vagina in the form of a waxy pessary or a cream.
Since irritation of the vulva is always associated with an intra-vaginal infection both areas
should be treated. One of the imidazole group of drugs usually proves to be effective in 90
per cent of women, as they have a wide range of action against yeasts and fungi. The more
popular clotrimazole (Canesten) may be given as 200 mg pessaries on three consecutive
nights or a single 500 mg pessary. Miconazole nitrate pessaries or cream (Gyno-Daktarin)
have a similar efficacy used over 14 nights, unlike the long-standing, cheaper fungicide
nystatin (80 per cent effective). In more resistant cases which have failed to respond to
vaginal threrapy, the oral administration of drugs such as ketoconazole (Nizoral),
itraconazole (Sporanox) and diflucan (Fluconazole) may have to be considered provided the
patient has no past history of hepatocellular damage.
INFECTION WITH TRICHOMONAS VAGINALIS
The infection is usually transmitted by a male carrier during sexual intercourse, but it may
also be carried on toilet articles from one woman to another. Cross-infection in antenatal and
gynaecological clinics may occur, and disposable gloves should be used for examination.
There is usually a profuse and offensive yellow frothy discharge which produces irritation
and soreness but in a few cases the discharge is less, and it is not sufficient to rely on nakedeye appearances for diagnosis.
The onset is sudden, and there may be a history of previous similar attacks. This infection
can occur in women of any age and is often seen during pregnancy.
There may be inflammation of the vulva and urethra and vaginal examination may be
difficult because of soreness. There is a profuse, frothy, thin greenish-yellow discharge
which has a characteristically unpleasant odour. The vaginal wall is intensely red and
inflamed and numerous minute punctate ulcers (strawberry spots) may be seen.
Diagnosis
The diagnosis is easily established in the clinic by examination of the discharge. A little of it
is taken, with a wire loop or pipette, and placed in a drop of normal saline on a glass slide
and, after covering with a coverslip, it is examined at once with a microscope, using a 4 mm
objective. If the specimen is examined without delay there is no need to warm the saline or
the slide. The pear-shaped protozoon (T. vaginalis) will be recognized by its high motility;
numerous leucocytes will also be seen. The trichomonads are a little larger than leucocytes,
and, if stained, they can be shown to have flagella at one end and a spear-like protrusion at
the other, hence the name from the Greek Trichos, a hair .
Treatment
Metronidazole (Flagyl) is given orally, 200 mg three times a day for a week. Since patients
are often reinfected by their sexual partners, the partner should also be given the same
treatment. Alternatively, 2 doses of 2 g may be given in one day, followed by 1 g daily for 7
days. Patients should avoid taking alcohol as they may suffer vomiting, headaches and
flushing. Subsequent recurrence of the infection calls for a further course of treatment and
examination of the consort; the Trichomonas may be found in the urethra or under the
prepuce. As it is not uncommon for women with Trichomonas infection to have gonorrhoea
as well, tests should be done to exclude gonococcal infection.
NON-SPECIFIC VAGINITIS
In the past this was the term used to describe a situation where there seemed to be no
infecting agent to account for the vaginitis. However, for infection occurring during the
reproductive years this label is inappropriate and every effort should be made to arrive at a
specific cause for the vaginitis. In some instances anaerobes in conjunction with G. vagmalis
may be responsible.
In the prepubertal and postmenopausal years, when the thin vaginal epithelium is susceptible
to various irritative phenomena or non-specific infective agents, the term non-specific
vaginitis may be applicable, although it is better to use more descriptive terminology to
describe the associations.
ATROPHIC VAGINITIS
After the cessation of menstruation slow atrophy occurs in the vulva and vagina. There is
thinning of the vulval and vaginal epithelium, loss of glycogen in the vaginal epithelial cells
and fall in acidity. Local resistance to infection is further diminished by the reduced blood
supply.
Treatment
When malignant disease has been excluded as a cause of the discharge, the vaginitis is
treated with oestrogens, such as ethinyloestradiol, 10 micro-grams by mouth twice a day for
14 days or by the instillation into the vagina of dienoestrol cream. Rapid regeneration of the
epithelium of the vagina and an increase in blood supply are to be expected, but
unfortunately endometrial bleeding may also occur. Unless this bleeding is of short duration,
and does not recur, diagnostic curettage must be performed. The possibility of bleeding may
be reduced, but not entirely eliminated, by administering the oestrogen in the form of creams
which act locally on the vaginal epithelium.
VULVOVAGINITIS IN CHILDHOOD
Because vaginitis in children is usually accompanied by secondary vulvitis, the term
vulvovaginitis is often used. Protection of the non-oestrogenized vagina by the hymen is
usually effective, but infection may occur as a result of poor hygiene, insertion of a foreign
body by the child or sexual interference. A few instances of streptococcal infection appear to
be associated with infections of the throat or scarlatina. Candi-diasis and trichomoniasis are
uncommon, but infection may be carried from an adult if the family standard of hygiene is
poor. Gonococcal infection may occur.
The child usually complains of soreness and discomfort on micturition. The vulval skin is
reddened, and discharge may be evident; but sometimes the discharge is only a slight stain on
clothing noticed by an anxious mother—she, rather than the child, may require reassurance.
A copious purulent discharge suggests the presence of a foreign body. Anal threadworms
may cause pruritus and scratching.
Treatment
Advice on hygiene may be necessary. The vulval region should be bathed daily, but irritant
antiseptics should not be added to the water, and care must be taken to rinse detergents out of
clothing.
It is seldom necessary to give an anaesthetic for examination; a small wire loop or pipette
may be passed into the vagina to obtain discharge for bateriological examination. A foreign
body may be felt by rectal examination, or possibly seen with the aid of a small nasal
speculum. Oestrogens may be tried (ethinyloestradiol, 5 mg daily by mouth for a small child)
or dienoestrol cream applied locally before a more thorough investigation. Trichomoniasis is
treated with oral metronidazole but with half the adult dose. Candidiasis is treated with oral
nystatin suspension (400 000 units per g three times daily).
OTHER CAUSES OF VAGINITIS AND VAGINAL DISCHARGE
CHEMICAL VAGINITIS
Vaginitis may result from direct or allergic reactions to chemicals in spermicides used in
barrier contraceptives or from agents contained in douches, deodorants, bath preparations and
certain condoms.
ACUTE CERVICITIS
The endocervical columnar epithelium may occasionally be infected by the gonococcus,
Chlamydia trachomatis or by a herpes or papilloma virus. Cervical infection may also follow
childbirth or operative dilatation of the cervix, and spread into the base of the broad ligament
(parametrium).
Although the cervix may appear reddened, congested and swollen, with a purulent exudate
from the canal and accompanying vaginal and urethral irritability, the condition is quite often
symptom-less. Acute cervicitis is seldom seen as an isolated condition, usually being found
in patients who have an acute infection elsewhere in the genitaltract. Treatment should be
directed to the particular infecting agent.
CHRONIC CERVICITIS
True cervical infection may persist after bacterial invasion at the time of delivery or abortion.
In such cases mucopus is seen coming from the external os. In addition to the discharge,
chronic cervicitis is often associated with pelvic pain, dys-pareunia and sometimes backache.
On examination the cervix is enlarged by multiple retention cysts of the cervical glands
(nabothian follicles) and these cysts may become secondarily infected.
An occasional specific cause of chronic cervicitis is infection with Chlamydia trachomatis
(detectable by special culture techniques). On rare occasions tuberculosis has also been found
to be the cause.
Management
A cervical smear should be taken for cytological examination and cervical and vaginal swabs
should be sent for bacteriological culture. Many cases may show only a mixed flora but
sometimes antibiotic therapy may be indicated for a specific infecting
organism. The most usual treatment is cauterization of the cervix, which may be done as an
outpatient without anaesthesia using cryosurgery, electrocautery or lasers to destroy the
superficial epithelium. However, more extensive lesions need to be treated under general
anaesthesia, allowing dilatation of the cervix and cauterization of the tissues to a depth of
about 2 mm. Separation of the necrotic tissue causes discharge for 2-3 weeks and
occasionally secondary haemorrhage may occur around the 1 Oth day as the slough is shed.
Cervical stenosis can occasionally be a late complication of cautery.
ENDOMETRITIS
During reproductive life endometritis is uncommon, except after delivery or abortion.
The cavity of the uterus is protected against bacterial invasion by the acid barrier of the vagina
and the cervical mucus, and in addition the shedding of the en-dometrium at each menstrual
period prevents organisms from gaining a foothold for long. However, after delivery or abortion
lochial discharge forms an excellent culture medium and organisms may enter the tissues at the
site from which the placenta has separated.
Endometritis may follow operations such as curettage, or the insertion of an intrauterine
device. When an intrauterine device is in place the subjacent endometrium shows infiltration
with polymorphonuclear leucocytes. This may merely be a response to the foreign body, but in a
few cases actinomyces-like organisms have been noticed in smears or cultured from the uterus.
Gonococcal infection may spread upwards from the cervix to the endometrium and tubes,
while tuberculosis endometritis often follows tuberculous salpingitis.
With advanced carcinoma of the endometrium or of the cervix, especially if the cervical
canal is obstructed, infection occurs.
After the menopause there may be ascending infection which causes what was formerly
called senile endometritis, now called atrophic endometritis.
PELVIC INFLAMMATORY DISEASE
Pelvic inflammatory disease (PID) is a clinical syndrome attributed to the ascending
spread of micro-organisms (unrelated to pregnancy or surgery) from the vagina and cervix to the
endometrium, fallopian tubes and or contiguous structures.
The clinical syndrome usually begins with an acute episode which can be followed either
by complete resolution or gradual subsidence into a more chronic process which may also
exhibit further acute or subacute resurgences. At the other extreme, however, it may be a
clinically benign condition which goes unrecognized and is only diagnosed when the damage has
been done and the woman is under investigation for infertility or has an ectopic pregnancy. It is
suggested that only a minority of women whose infertility is due to tubal damage give a history
of previous overt disease.
Diagnosis of pelvic inflammatory disease
Even experienced gynaecologists have difficulty in correctly diagnosing PID; the
symptoms are often unreliable. Hare (1986) produced an algorithm for pelvic inflammatory
disease. He advised that unless three or more of his listed symptoms were present, in addition to
abdominal pain and dyspareunia, the diagnosis must remain uncertain. He felt that signs were
more usual than symptoms, but at least three signs should be elicited. Obviously if doubt remains
laparoscopy should be performed—both for the immediate safety of the patient, in making the
correct diagnosis, and for planning treatment.
ACUTE SALPINGITIS
Pathology
In acute salpingitis both tubes are congested, red and oedematous and there is usually a
seropurulent exudate. The plicae of the tubal mucosa are swollen, and the epithelium covering
them is shed in places. It is possible for this type of inflammation to subside without leaving any
gross changes, but in most cases damage is done to the ciliated epithelium of the tube, causing
infertility or a delay in the transport of the fertilized ovum and therefore an ectopic pregnancy.
The infected tube frequently becomes occluded. The lumen of the interstitial part is so
fine that the slightest inflammatory reaction blocks it. The fimbriae adhere at the other end of the
tube and are drawn into the tube, and the abdominal ostium is sealed. Once the ends are closed,
inflammatory exudate collects and distends the tube. When the collection of fluid is more or less
clear it is called a hydrosalpinx, when it is purulent, a pyosalpinx. Because the ampullary end of
the tube distends more easily than the isthmus the tube becomes retort-shaped If the infecting
organisms are virulent they can pass deep into the wall of the tube, which becomes thickened,
and as the covering peritoneum becomes involved in the inflammation peritoneal adhesions
occur.
The ovaries are also affected by the inflammation. They become enlarged by oedema and
adhere to the fallopian tubes by filmy adhesions. If the infection is severe the ovary develops
small abscesses, or may form part of the wall of an abscess cavity with the tube and adjacent
structures. A distended tube may communicate with a cyst of the ovary, forming a tubo-ovarian
abscess.
In some cases the inflammation does not result in the collection of pus within the lumen
of the tube. Inflammatory changes within the muscle wall produce areas of variable thickening
and fibrosis, often with kinking. This condition is called interstitial salpingitis, and is often
found as a residual lesion in patients whose symptoms have resolved.
Symptoms and signs
The patient feels ill and complains of lower abdominal pain, which is worse on
movement. Vomiting may occur at the onset and the bowels are constipated. The pulse rate is
increased and the temperature is raised, often above 39.5°C. The tongue is dry but not usually
furred. Because there is pelvic hyperaemia there may be a mucous discharge from the uterus
which may be purulent if there is cervicitis or infection by Trichomonas vaginalis. Because there
is oophoritis the menstrual cycle is often upset. In many cases in which the infection is of low
virulence all symptoms disappear in a few days, and the true nature of the illness is never
discovered.
Examination shows tenderness and rebound tenderness over the pelvis and both iliac
fossae. If peritonitis is present there may be rigidity and abdominal distension over the lower
abdomen. Pelvic examination causes pain, especially on movement of the uterus. In many cases
the tenderness in the fornices is such that no other physical signs can be made out. In less acute
cases a sense of fullness is noticed in the lateral fornices on bi-manual examination. The
converse is perhaps more useful; if bimanual pressure to the side of the uterus is not painful, the
patient is certainly not suffering from acute salpingitis.
If there is a peritubal abscess, the encysted serous peritonitis around it forms a mass,
which may become palpable above the symphysis pubis.
It is irregular in outline and partly resonant on percussion because of adhering coils of
intestine. In order to relax the abdominal muscles over this tender mass the patient often lies in
bed with both knees flexed.
Abscess formation, inside or outside the tube, is accompanied by deterioration of the
patient's condition. She looks and feels ill, and complains of increasing pain. Her appetite
deteriorates and she sleeps badly. Temperature and pulse rate increase and rigors may occur;
there is increasing leuco-cytosis. The pelvic mass increases in size, and if left alone the abscess
usually points and drains into the rectum; this event is often preceded by mucous diarrhoea.
With modern antibiotic treatment the formation of a large pelvic mass is seen less often
than it used to be, and, left alone, it tends to absorb after one or two weeks. The tender fallopian
tubes may then be felt as oblong, tender, fixed masses behind the uterus. The patient may be left
with blocked tubes and more or less dense pelvic adhesions.
Diagnosis
At its onset acute salpingitis must be distinguished from acute appendicitis. If the
appendix is pelvic, the signs may be similar.
The history will often be helpful, for in salpingitis there will generally be history and
signs of recent abortion or delivery or of gonococcal infection.
In appendicitis the pain usually starts near the umbilicus and later becomes localized to
the right iliac fossa; in salpingitis the pain starts in the lower abdomen and is bilateral. The
temperature with salpingitis is usually higher, often reaching 39.5°C, whereas in appendicitis it
seldom exceeds 38.5°C;the pulse rate, however, is not as high in salpingitis as in appendicitis.
Vomiting may occur with either condition but is more constant with appendicitis. A furred
tongue suggests appendicitis. In cases of salpingitis, vaginal examination shows tenderness in
both lateral fornices; in appendicitis the signs will be more marked on the right side. If a
pyosalpinx has formed, the history will usually make the nature of the swelling obvious.
However, if the patient is first seen at this stage, the swelling will have to be differentiated from
an ectopic gestation with a tubal mole or from a small ovarian cyst.
Treatment
Bed rest, adequate fluid intake and analgesics are the basic necessities in the treatment of
acute salpingitis, but the selection of suitable antibiotics, in adequate dosage, is also essential.
Should an intrauterine contraceptive device be in place it should be removed after antibiotic
cover is achieved.
Bacterial swabs are taken from the cervix and urethra and should be tested for Chlamydia
and, although gonococcal salpingitis is now less common in the UK, this must also be excluded.
However, treatment should be carried out without waiting for a bacteriological report, so as to
avoid permanent damage to the tubes.
There is no ideal antibiotic regime for the treatment of salpingitis. Treatment should
begin with a single (antigonococcal) dose of spectinomycin (2 g intramuscularly) or cefuroxime
(1.5 g intramuscu-larly), followed by a tetracycline (e.g. oxytetracy-cline 500 mg four times
daily by mouth, or doxy-cycline 100 mg twice daily by mouth), plus oral metronidazole 400 mg
daily for 14 days. Initial parenteral therapy (tetracycline hydrochloride 500 mg 12 hourly
intravenously plus metronidazole 500 mg intravenously or per rectum) may be required in severe
cases. Pregnant patients, or those who are intolerant of tetracyclines, should be given
erythromycin stearate 500 mg four times daily by mouth, plus metronidazole as above for 14
days. However, this latter regimen will not be effective against Mycoplasma hominis, and is
unreliable for N. gonorrhoeae.
Recurrent PID is not uncommon and the risk of infertility or ectopic pregnancy increases
with further episodes of infection. It is therefore important to trace the patient's contacts, and her
partners should be referred to a genitourinary medicine clinic for investigation and treatment.
Surgical treatment of acute salpingitis is seldom called for and if laparotomy (performed
when the diagnosis is doubtful and appendicitis may be a possibility) shows that the tubes are
acutely inflamed, they should not be removed if there is any hope of restoration of function.
Bacterial swabs should be taken from any pus and from the lumen of the tubes before closing the
abdomen.
Surgery may be contemplated in the very rare cases of deterioration in spite of active
medical forms of treatment. When there is definite evidence of a pelvic abscess, this must be
drained. Where the patient suffers from repeated recurrent attacks of acute salpingitis the tubes
become irretrievably blocked and their removal during a quiescent phase is advised.
CHRONIC SALPINGITIS
An abscess often does not form after an attack of acute salpingitis, yet the disease
obviously fails to resolve completely. A patient with chronic salpingitis may be ambulant and
even follow her regular employment. However, she does not feel well and many ordinary daily
tasks become a burden. The menstrual loss is often heavy and is preceded by congestive
dysmenorrhoea with pain which precedes, and lasts throughout, each period.
The inflammation of the ovaries may upset the menstrual cycle and produce irregular
bleeding. In addition to menstrual pain there is often continuing dull pain or aching in the lower
abdomen or back. There is dyspareunia and there may be an excessive cervical discharge. On
pelvic examination there is tenderness and residual thickening of one or both tubes, or a fixed
tender mass in the rectouterine pouch of Douglas due to bilateral pyosalpinges. Ovarian
endometriomatous cysts may cause pelvic pain and menorrhagia, and the physical signs closely
resemble those of chronic salpingitis with bilateral tubal swellings. The absence of a history of
infection after abortion or delivery, gonorrhoea, any suggestion of tuberculosis and the absence
of pyrexia, help in reaching the correct diagnosis.
Treatment
Only prolonged antibiotic therapy and convalescence have any prospect of resolving this
condition. It may be necessary to continue treatment for 3-6 months, changing between the
various broad spectrum antibiotics.
Often these measures fail and surgical treatment is indicated. While healthy tissue should
obviously be conserved, the patient should not be left with infected tissues which will need
further surgical treatment. This means that both tubes may have to be removed, and in such
cases, especially if there is menorrhagia and discharge, total hysterectomy is often wise. An
effort should be made to find and conserve any healthy ovarian tissue.
Tuberculous infection of the genital tract is becoming uncommon in the UK; it is seen
more often in developing countries. The infection is a chronic one, and is almost invariably
secondary to a tuberculous infection in the lung, although by the time the genital infection
becomes manifest the primary lesion may be quiescent or healed. Although it is theoretically
possible for a patient to be infected directly from a male with tuberculous epididymitis, this
event is almost unknown.
The fallopian tube is the most common site of initial infection in the pelvic organs.
Diagnosis
Since, in nearly every case of active tuberculous salpingitis, the endometrium is involved,
histolo-gical examination of curettings will show the presence of tubercles. Part of the material
removed by currettage is sent for bacterial culture or guinea-pig Fig. 5.6 Bilateral tuberculous
pyosalpinges. The walls of both tubes are thickened and they contain caseous material. Tubercles
are seen on the peritoneal surface inoculation. In every case a radiological examination of the
chest must be made.
Treatment
It is recommended that extrapulmonary tuberculosis should be treated in the same way as
pulmonary tuberculosis. Several drugs are given in combination to prevent the emergence of
resistant strains. Use of an intensive four-drug regimen (for example, rifampicin, isoniazid,
ethambutol and pyrazinamide) for 8 weeks allows the total treatment to be reduced to 6 months.
Infections of the Upper Genital Tract

Pelvic inflammatory disease (PID) is an infection of the upper genital tract. The disease
process may include the endometrium, fallopian tubes, ovaries, myometrium,
parametrium, and pelvic peritoneum.
o Pathophysiology and Microbiology. PID is caused by the spread of infection via
the cervix. Although PID is associated with sexually transmitted infections of the
lower tract, its process is polymicrobial. N. gonorrhoeae or C. trachomatis are
implicated in many cases, but numerous micro-organisms may be involved. A
positive endocervical culture result for a particular pathogen does not necessarily
correlate with positive intra-abdominal culture findings.
o Prevention. Emphasis must be placed on aggressive treatment of lower genital
tract infection and early aggressive treatment of upper genital tract infection. This
helps reduce the incidence of long-term sequelae. Treatment of sexual partners
and education is important in reducing the rate of recurrent infections.
o Risk factors include a previous history of PID, multiple sex partners, defined as
more than two partners in 30 days, and infection by a sexually transmitted
organism. Use of an IUD can increase the risk of PID by up to six times but only
within the first 3 weeks after placement. Thereafter, the risk is relatively low (10).
Use of nonbarrier contraception is also a developing risk factor.
o Signs and Symptoms. The most common presenting symptom is abdominopelvic
pain. Other complaints are variable, including vaginal discharge or bleeding, fever
and chills, nausea, and dysuria.
o Diagnosis of PID is difficult because the presenting signs and symptoms vary
widely. Because of the sequelae of PID, especially infertility, ectopic pregnancy,
and chronic pelvic pain, health care providers should maintain a low threshold for
diagnosis PID (4).
 Minimal Criteria. Empiric treatment should be initiated in young women
at risk for STDs if they are experiencing pelvic or lower abdominal pain,
if no other cause can be identified, and if one or more of the following are
present on pelvic examination:
 Cervical motion tenderness
 Uterine tenderness
 Adnexal tenderness
 Additional Criteria for Diagnosis
 Oral temperature >101В°F (>38.3В°C)
 Abnormal cervical or vaginal mucopurulent discharge


Presence of white blood cells on saline microscopy of vaginal
secretions
 Elevated erythrocyte sedimentation rate
 Elevated C-reactive protein
 Laboratory documentation of cervical infection with N.
gonorrhoeae or C. trachomatis
 Specific Criteria for PID
 Endometrial biopsy with histopathologic evidence of endometritis
 Transvaginal sonography or magnetic resonance imaging
techniques showing thickened, fluid-filled tubes with or without
free pelvic fluid or tubo-ovarian complex
 Laparoscopic abnormalities consistent with PID
o Treatment for PID should have as its goals the prevention of tubal damage that
leads to infertility and ectopic pregnancy and prevention of chronic infection.
Many patients can be successfully treated as outpatients, and early ambulatory
treatment should be the initial therapeutic approach. Antibiotic choice should
target the major etiologic organisms (N. gonorrhoeae and C. trachomatis) but
should also address the polymicrobial nature of the disease (Tables 24.11 and
24.12).
 Criteria for Hospitalization
 Surgical emergencies (e.g., appendicitis) should not be excluded.
 The patient is pregnant.
 The patient does not respond clinically to oral antimicrobial
therapy.
 The patient is unable to follow or tolerate an outpatient oral
regimen.
 The patient has severe illness, nausea and vomiting, or high fever.
 The patient has a tubo-ovarian abscess.
o Sequelae. Approximately 25% of PID patients experience long-term sequelae.
Infertility due to tubal occlusion affects anywhere from 6% to 60% of women
following an episode of PID, depending on severity, whereas the risk of ectopic
pregnancy is approximately 6 to 10 times normal. Chronic pelvic pain and
dyspareunia have also been reported. Fitz-Hugh-Curtis syndrome is the
development of fibrous perihepatic adhesions resulting from the inflammatory
process of PID. This can cause acute right upper quadrant pain and tenderness.
Endometritis (Nonpuerperal)
o Pathophysiology. Endometritis is caused by the ascension of pathogens from the
cervix to the endometrium. Pathogens include C. trachomatis, N. gonorrhoeae,
Streptococcus agalactiae, cytomegalovirus, HSV, and Mycoplasma hominis.
Organisms that produce bacterial vaginosis may also produce histologic
endometritis, even in women without symptoms. Endometritis is also an
important component of PID and may be an intermediate stage in the spread of
infection to the fallopian tubes.
o Signs and Symptoms
 Chronic Endometritis. Many women are asymptomatic. The classic
symptom of chronic endometritis is intermenstrual vaginal bleeding.
Postcoital bleeding, menorrhagia, and a dull, constant lower abdominal
pain are other complaints.
 Acute Endometritis. Uterine tenderness is common.
o Diagnosis. The diagnosis of chronic endometritis is established by endometrial
biopsy and culture. The classic histologic findings of chronic endometritis are an
inflammatory reaction of monocytes and plasma cells in the endometrial stroma
o
(five plasma cells per high-power field). A diffuse pattern of inflammatory
infiltrates of lymphocytes and plasma cells throughout the endometrial stroma or
even stromal necrosis is associated with severe cases of endometritis.
Treatment. The treatment of choice for chronic endometritis is doxycycline, 100
mg PO bid for 10 days. Broader coverage of anaerobic organisms may also be
considered, especially in the presence of bacterial vaginosis. When endometritis is
associated with acute PID, treatment should focus on the major etiologic
organisms, including N. gonorrhoeae and C. trachomatis, and should also include
broader polymicrobial coverage.
V. Self-assessment tasks:
1. What is premature development?
2. Methods of diagnostics of premature sexual development.
3. Make a plan to treat the patient with premature sexual development.
4. What is sexual development delay? Clinical picture.
5. Methods of diagnostics and treatment of syndrome of sexual development delay.
6. Classification of inflammatory gynaecological diseases in girls and juvenile.
7. What is vulvovaginitis? Clinical picture, diagnostics and treatment.
8. Methods of diagnostics of vulvovaginitis.
9. Clinical picture of vulvovaginitis.
10.Diagnostics of vulvovaginitis.
11. Prescribe the treatment of vulvovaginitis in accordance with age.
12. Classification of inflammatory gynaecological diseases in girls and juvenile.
13. Clinical picture, diagnostics of inflammatory diseases of internal genitals in girls and
juvenile.
14. Methods of diagnostics of clamidiosis.
15. Prescribe the treatment of clamidiosis in accordance to age.
16. What is ureaplasmatic vulvovaginitis? Clinical picture, diagnostics of treatment.
17. What is gardnerelosis? Methods of its diagnostics in girls and juvenile and its treatment.
18. Bacterial vaginosis. Methods of its diagnostics and treatment in juvenile.
VI. Literature.
1. American Academy of Pediatrics Committee on Quality Improvement, Subcommittee on
Urinary Tract Infection. Practice Parameter: The diagnosis, treatment and evaluation of the
initial urinary tract infection in febrile infants and young children. Pediatrics
1999;103;4:843–852.
2. Sanfilippo JS. Pediatric and Adolescent Gynecology, 2nd Ed. Philadelphia: WB Saunders,
2001:227–231.
3. Reiter EO, Lee PA. Adolescent endocrinology: delayed puberty. Adolesc Med 2002;13
(1):101–118.
4. Larsen PR. Williams Textbook of Endocrinology, 10th Ed. Elsevier, 2003:1171–1202.
5. Stenchever MA. Comprehensive Gynecology, 4th Ed. Mosby, 2001:280–288.
6. Kaplowitz PB. Reexamination of the age limit for defining when puberty is precocious in girls
in the United States: implication for evaluation and treatment. Drug and Therapeutics and
Executive Committees of the Lawson Wilkins Pediatric Endocrine Society. Pediatrics 1999;104
(4 Pt 1):936–941.
7. Antoniazzi F, Zamboni G. Central precocious puberty: current treatment options. Paediatr
Drugs 2004;6 (4):211–231.
8. Speroff L, Glass RH, Kase NG. Clinical Gynecologic Endocrinology and Infertility, 5th Ed.
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