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Pemicu 5

Blok Reproduksi
Aldi Firdaus
405140098
LI
1. Kelainan Ginekologi krn Infeksi
2. Kelainan Ginekologi krn Kelainan Organ Genitalia
3. Kelainan Ginekologi krn Tumor
4. Infertilitas
SALFINGITIS/ADNEKSITI
S
Definis
i
• Salfingitis: Infeksi pada tuba falopii
• Oophoritis: Infeksi pada ovarium
• Adneksitis: Infeksi pada tuba falopii dan ovarium

 Merupakan infeksi tinggi/infeksi radang panggul yang


paling sering
Klasifika
si
• Salfingitis/adneksitis akut
– Disebabkan oleh Gonorrhoe (60% disebabkan oleh GO) dan kuman-
kuman lain seperti Streptococcus aerob dan Staphylococcus
anaerob
• Salfingitis/adneksitis kronik
– Dari radang akut atau infeksi kuman tuberkulosis
Faktor Risiko
Infeksi
• Menstruasi
• Partus
• Abortus
• Operasi ginekologis/kuretase
• Alat kontrasepsi dalam rahim
(AKDR)
Salfingitis/Adneksitis
Akut
• Etiologi: Paling sering disebabkan oleh gonokokus
• Patofisiologi infeksi: Infeksi dapat terjadi sebagai berikut:
– Naik dari cavum uteri
– Menjalar dari alat yang berdekatan seperti dari appendiks
yang meradang
– Hematogen terutama pada salfingitis tuberkulosis (biasanya
bilateral)
• Gejala-gejala:
– Demam tinggi dengan menggigil
– Pasien tampak sakit keras
– Nyeri kiri dan kanan perut bagian bawah
terutama saat perut ditekan
– Mual dan muntah
– Akut abdomen (terjadi karena iritasi peritoneum)
– Tenesmus ani karena proses peradangan
mengiritasi rektum/kolon sigmoid
– Menorrhagi
– dysmenorrhoe
– Dyspareunia
• Pemeriksaan fisik:
– Pemeriksaan abdomen:
• Nyeri tekan perut kiri dan kanan bagian bawah
• Defense kiri dan kanan diatas ligamentum inguinal
– Vaginal toucher:
• Nyeri kalau portio digoyangkan
• Nyeri kiri dan kanan dari uterus
• Teraba penebalan dari tuba (tuba yang sehat tidak
dapat diraba)
• Teraba tumor adneksa karena terjadi perlekatan
adneksa dengan usus akibat radang
*) Tekanan pada ovarium selalu menimbulkan nyeri
walaupun
ovarium tidak meradang
• Pemeriksaan laboratorium:
– LED meningkat
– Leukositosis
– Tes kehamilan negatif
• Pemeriksaan USG
• DD/:
– Kehamilan ektopik:
• Biasanya tidak ada demam, LED tidak meninggi,
leukositosis tidak seberapa, tes kehamilan
positif
– Appendisitis:
• Nyeri tekan khas pada titik McBurney
• Terapi:
– Istirahat
– Puasa
– Spektrum luas
antibiotika
– Kortikosteroid
Salfingitis/Adneksitis
Kronik
• Patofisiologi: Infeksi terjadi akibat:
– Sebagai lanjutan dari adneksitis akut
– Dari permulaan sifatnya sudah kronik seperti adneksitis tuberkulosa
(adneksitis
pada seorang perawan harus menimbulkan kecurigaan adneksitis tuberkulosa)
• Gejala-gejala:
– Anamnesis telah menderita adneksitis akut sebelumnya
– Nyeri di perut bagian bawah atau pinggang: nyeri bertambah sebelum
dan sewaktu haid atau waktu buang air besar
– Dysmenorrhoe
– Menorrhagi
– Infertilitas
• Pemeriksaan fisik:
– Pemeriksaan abdomen:
• Nyeri perut kanan atau kiri bagian bawah
• Teraba tumor pada perut kanan atau kiri bagian
bawah
– Rectal toucher:
• Teraba tumor adneksa
• Pemeriksaan laboratorium:
– LED meninggi
– Leukositosis
– Limfositosis
• Pemeriksaan USG
• DD/:
– Appendisitis kronik
– Kehamilan ektopik yang terganggu
• Terapi:
– Istirahat
– Puasa
– Spektrum luas antibiotika
– Kalau tidak ada perbaikan dipertimbangkan
terapi operatif
Abses Tubo-
Ovarium
• Nama lain: Pyosalpinx dan pyovarium
• Definisi: Terbentuk kantong berisi pus akibat peradangan
pada tuba falopi atau ovarium
• Diagnosis: Terdapat riwayat salfingitis sebelumnya
disertai gejala nyeri perut bawah
• Pemeriksaan fisik:
– Pemeriksaan abdomen: Nyeri tekan dan adanya tumor adneksa
pada perut bagian bawah kiri dan kanan
– Vaginal toucher: Teraba tumor adneksa dan nyeri
• Pemeriksaan laboratorium:
– LED meninggi
– Leukositosis
– Limfositosis
• Pemeriksaan USG: Dilakukan untuk
menegakkan diagnosis dari abses
tubo- ovarium
• Terapi:
– Istirahat
– Puasa
– Spektrum luas antibiotika parenteral
– Drainase abses dipandu dengan USG atau CT-scan
– Kalau tidak ada perbaikan dipertimbangkan
terapi operatif
• Komplikasi:
– Terjadi akibat rupturnya abses atau nanah yang
masuk ke rongga perut melalui ujung tuba
– Peritonitis
– Abses Douglas
Terapi
Parenteral
Terapi
Oral
Referens
i
• Bagian Obstetri dan Ginekologi Fakultas Kedokteran
Universitas Padjadjaran Bandung. Ginekologi. 2nd ed. Bandung:
CV. Lubuk Agung; 2010.
• https://www.cdc.gov/std/treatment/2010/pid.htm
• http://emedicine.medscape.com/article/404537-overview
Cervicitis
Cervicitis
Cervicitis is an inflammation of the uterine
cervix, characteristically diagnosed by:
•a visible, purulent or mucopurulent
endocervical exudate in the
endocervical canal or on an endocervical swab
specimen and/or
•sustained, easily induced endocervical bleeding when a cotton
swab is gently passed through the cervical os.

https://www.cdc.gov/std/tg2015/urethritis-and-cervicitis.htm
Cervicitis: etiology
The most common etiologies of cervicitis are infectious, with
sexual transmission of organisms such as with C trachomatis
and N gonorrhoeae being the primary means by which it is
spread.

Other etiologic organisms include Trichomonas vaginalis


and herpes simplex virus (HSV), especially primary type 2
HSV

https://www.cdc.gov/std/tg2015/urethritis-and-cervicitis.htm
Cervicitis: etiology
•Noninfectious causes of cervicitis include local trauma, radiation,
chemical irritation, systemic inflammation, and malignancy.
•Limited data exist to suggest frequent douching, as well as
Mycoplasma genitalium infection and bacterial vaginosis, as
potential causes

For reasons that are unclear, cervicitis can persist despite repeated courses of antimicrobial
therapy. Because most persistent cases of cervicitis are not caused by recurrent or reinfection
with C. trachomatis or N. gonorrhoeae,

https://www.cdc.gov/std/tg2015/urethritis-and-cervicitis.htm
Cervicitis
The cervix is made up of two different types of epithelial cells:
squamous epithelium and glandular epithelium. The cause of cervical
inflammation depends on the epithelium affected.
The ectocervical epithelium can become inflamed by the
same microorganisms that are responsible for vaginitis.
In fact, the ectocervical squamous epithelium is an extension of and is
continuous with the vaginal epithelium. Trichomonas, candida, and HSV
can cause inflammation of the ectocervix.
Conversely, N. gonorrhoeae and C. trachomatis infect only the
glandular epithelium

Berek & Novak’s Gynecology, 14th edition, 2007


Cervicitis: Risk Factors
Risk factors for cervicitis include the
following: Multiple sex partners
Young age
Single marital
status Urban
residence Low
socioeconomic
Alcohol or drug use
http://emedicine.medscape.com/article/253402-overview#a4
Cervicitis: Signs-Symptoms
Cervicitis is often asymptomatic in gonorrhea, chlamydia, and
T vaginalis infections. When present, symptoms are often
nonspecific and may include increased vaginal discharge,
dysuria, urinary frequency, and intermenstrual or postcoital
bleeding.

https://www.cdc.gov/std/tg2015/urethritis-and-cervicitis.htm
Cervicitis: Signs-Symptoms
A focused review of symptoms is recommended that asks
about
the following:
Dyspareunia
Vaginal discharge
Genital skin
lesions
Abnormal vaginal
bleeding
Dysuria
Genital burning
Genital itching
Genital
malodor https://www.cdc.gov/std/tg2015/urethritis-and-cervicitis.htm
Cervicitis: Physical
Exam
The physical examination should include a
general survey, an external inspection, and
pelvic speculum and bimanual
examinations.

https://www.cdc.gov/std/tg2015/urethritis-and-cervicitis.htm
Speculum examination
Normal vaginal secretions are nonadherent to the
vaginal walls, clear to white in color, and nonodorous.
Normal vaginal secretions have an acidic pH of less than
4.5.
Vaginitis is present if the vaginal discharge is copious,
colored, and malodorous, or if the pH is greater than
4.5.
Cervicitis is suspected if the cervix is erythematous,
edematous, or easily friable. Classic mucopurulent
cervicitis is present if thick, yellow-green pus is visible in
the endocervical canal or on an endocervical swab
specimen. Laboratory specimens are collected for study
at this point. Note cervical warts or ulcerations.
http://emedicine.medscape.com/article/253402-clinical#b3
Bimanual Exam
Bimanual examination is performed to assess
tenderness or enlargement of the cervix,
uterus, and adnexa.
Cervicitis or pelvic inflammatory disease (PID) is
suspected if the patient has cervical motion
tenderness (ie, if she experiences pain or
tenderness while the examiner gently moves
the cervix from side to side).

http://emedicine.medscape.com/article/253402-clinical#b3
Cervicitis:
Treatment
In women of childbearing age, always perform a
urine pregnancy test before prescribing any
medication

http://emedicine.medscape.com/article/253402-overview#a4
Cervicitis:
Diagnosis
The diagnosis of cervicitis is based on the finding of a
purulent endocervical discharge, generally yellow or green
in color and referred to as “mucopus”

Berek & Novak’s Gynecology, 14th edition, 2007


Cervicitis: Diagnosis
Placement of the mucopus on a slide that can
be Gram stained will reveal the presence of an
increased number of neutrophils (30 per high-
power field).
The presence of intracellular gram-negative
diplococci, leading to the presumptive diagnosis
of gonococcal endocervicitis, also may be
detected. If the Gram stain results are negative
for gonococci, the presumptive diagnosis is
chlamydial cervicitis.
Berek & Novak’s Gynecology, 14th edition, 2007
Cervicitis: Treatment

Berek & Novak’s Gynecology, 14th edition, 2007


PID (Pelvic Inflammatory Disease)
PID
PID is caused by micro-organisms colonizing the endocervix
ascending to the disease endometrium and fallopian tubes. It
is a clinical diagnosis implying that the patient has upper
genital tract infection and inflammation. The inflammation
may be present at any point along a continuum that includes
endometritis, salpingitis, and peritonitis

Berek & Novak’s Gynecology, 14th edition, 2007


PID
•Pelvic inflammatory disease (PID) is an infectious and
inflammatory disorder of the upper female genital tract,
including the uterus, fallopian tubes, and adjacent pelvic
structures.
•Infection and inflammation may spread to the abdomen, including
perihepatic structures (Fitz-Hugh−Curtis syndrome)

http://emedicine.medscape.com/article/256448-overview
PI
D
Pelvic inflammatory disease commonly is caused by the
sexually transmitted micro-organisms N. gonorrhoeae and C.
trachomatis

Berek & Novak’s Gynecology, 14th edition, 2007


PID
• Endogenous microorganisms found in the vagina,
particularly the BV micro-organisms, also often
are isolated from the upper genital tract of
women with PID. The BV micro-organisms
include anaerobic bacteria such as Prevotella
and peptostreptococci as well as G. vaginalis. BV
often occurs in women with PID, and the
resultant complex alteration of vaginal flora may
facilitate the ascending spread of pathogenic
bacteria by enzymatically altering the cervical
mucus barrier.

Berek & Novak’s Gynecology, 14th edition, 2007


PID
• Less frequently, respiratory pathogens such as
Haemophilus influenzae, group A streptococci, and
pneumococci can colonize the lower genital tract and
cause PID.

Berek & Novak’s Gynecology, 14th edition, 2007


PID: Pathophysiology
Most cases of PID are presumed to occur in 2 stages. The
first stage is acquisition of a vaginal or cervical infection.
This infection is often sexually transmitted and may be
asymptomatic.
The second stage is direct ascent of microorganisms from
the vagina or cervix to the upper genital tract, with
infection and inflammation of these structures.

http://emedicine.medscape.com/article/256448-overview#a3
PID: Risk Factors
The classic patient at high risk for pelvic inflammatory disease
(PID) is a menstruating woman younger than 25 years who has
multiple sex partners, does not use contraception, and lives in
an area with a high prevalence of sexually transmitted
infections (STIs).
Young age at first intercourse is also a risk factor for PID. Use
of an intrauterine device (IUD) for contraception confers a
relative risk of 2.0-3.0 for the first 4 months following
insertion, but risk subsequently decreases to baseline.
Follow-up is recommended within the first month after IUD
insertion.

http://emedicine.medscape.com/article/256448-clinical
Tubo-Ovarian Abcess
•An end-stage process of acute PID, tubo-ovarian abscess is diagnosed
when a patient with PID has a pelvic mass that is palpable during
bimanual examination. The condition usually reflects an
agglutination of pelvic organs (tube, ovary, bowel) forming a
palpable complex.

Berek & Novak’s Gynecology, 14th edition, 2007


Tubo-Ovarian Abcess
Occasionally, an ovarian abscess can result from the entrance
of micro-organisms through an ovulatory site. Tubo-ovarian
abscess is treated with an antibiotic regimen administered in
a hospital. About 75% of women with tubo-ovarian abscess
respond to antimicrobial therapy alone. Failure of medical
therapy suggests the need for drainage of the abscess.

Berek & Novak’s Gynecology, 14th edition, 2007


PID: Signs and Symptoms

Berek & Novak’s Gynecology, 14th edition, 2007


PID: Signs and Symptoms

Some women may develop PID without having any symptoms.


Evaluation of both vaginal and endocervical secretions is a
crucial part of the workup of a patient with PID.
In women with PID, an increased number of
polymorphonuclear leukocytes may be detected in a wet
mount of the vaginal secretions or in the mucopurulent
discharge.

Berek & Novak’s Gynecology, 14th edition, 2007


PID: Signs and
Symptoms
All female patients of childbearing age with lower abdominal
pain require a pregnancy test. PID is the most common
incorrect diagnosis in missed ectopic pregnancy.

http://emedicine.medscape.com/article/256448-workup
PID: Diagnosis
Traditionally, the diagnosis of PID has been based on a triad of
symptoms and signs, including pelvic pain, cervical motion
and adnexal tenderness, and the presence of fever.

It is now recognized that there is wide variation in many


symptoms and signs among women with this condition,
which makes the diagnosis of acute PID difficult.

Berek & Novak’s Gynecology, 14th edition, 2007


For outpatient treatment, the CDC lists 2 currently accepted
treatment regimens, labeled as A and B.
Regimen A consists of the following:
•Ceftriaxone 250 mg intramuscularly (IM) once as a single dose plus
•Doxycycline 100 mg orally twice daily for 14 days
•Metronidazole 500 mg orally twice daily for 14 days can be added if there is
evidence or suspicion of vaginitis or if the patient underwent gynecologic
instrumentation in the preceding 2-3 weeks

https://www.cdc.gov/mmwr/pdf/rr/rr5912.pdf
For outpatient treatment, the CDC lists 2 currently accepted treatment
regimens, labeled as A and B.

Regimen B consists of the following:


•Cefoxitin 2 g IM once as a single dose concurrently with probenecid 1 g orally in
a single dose, or another single-dose parenteral third-generation cephalosporin
(eg, ceftizoxime or cefotaxime) plus
•Doxycycline 100 mg orally twice daily for 14 days
•Metronidazole 500 mg orally twice daily for 14 days can be added if there is
evidence or suspicion of vaginitis or if the patient underwent gynecologic
instrumentation in the preceding 2-3 weeks

https://www.cdc.gov/mmwr/pdf/rr/rr5912.pdf
BARTHOLIN GLAND DUCT CYST
AND ABSCESS
BARTHOLIN GLAND DUCT CYST AND
ABSCESS
• Mucus produced to moisten the vulva originates in part
from the Bartholin glands.
• Obstruction of this gland's duct can lead to cystic
enlargement that accounts for nearly 2 percent of all new
gynecologic visits (Fig. 4-9).
• Cysts may become infected, and the purulent contents result
in abscess development.
PATHOPHYSIOLOGY
• Infection
• Bartholin duct cysts form in direct response to obstruction of ductal outflow.
• Despite this understanding, the primary reason for cyst formation remains unknown.
• Abscess formation tends to develop in populations with demographic profiles similar to
those at high risk for sexually transmitted infections
• Historically, women with bilateral Bartholin gland duct cysts were assumed to have been
infected with Neisseria gonorrhoeae .
• However, resent studies have demonstrated a wider spectrum of organisms responsible
for
these cysts and abscesses.
• For example, Tanaka and colleagues (2005) examined 224 patients and approximately
two bacterial species per case were isolated. A majority were caused by aerobic
bacteria, of which Escherichia coli was the most common isolate.
• Interestingly, only five cases involved N gonorrhoeae or Chlamydia trachomatis
• Other theories for ductal obstruction include a change in
mucus consistency, mechanical trauma from poorly
repaired episiotomies, or even congenitally narrowed
ducts.
• Since mucus retention leads to cyst distention, the size
and speed of growth are influenced by sexual
stimulation.
• Hence, rapid accumulation is observed during times
of heightened sexual excitement.
• Malignancy
• After menopause, Bartholin gland duct cysts and abscesses are
uncommon and should raise suspicion of neoplasia.
• Carcinoma of the Bartholin gland is rare, and its incidence approximates
0.1 per 100,000 women.
• A majority of lesions are squamous carcinomas or
adenocarcinomas (Copeland, 1986).
• Given the rarity of these cancers, Bartholin gland excision is typically
not indicated.
• Alternatively, in women older than 40 years, drainage of the cyst
and biopsy of suspicious cyst wall sites adequately excludes
malignancy
Symptom
s
• Most Bartholin gland cysts are small and asymptomatic
except for minor discomfort during sexual arousal.
• When a lesion becomes larger or infected, women
may experience severe vulvar pain the precludes
them from walking, sitting, or engaging in sexual
activity.
Diagnosi
s
• A Bartholin gland enlargement can mimic several other
vulvovaginal masses.
• Most cysts are unilateral, round or ovoid, and tense.
• Abscesses typically display surrounding erythema and are tender
to palpation.
• The mass is usually located in the posterior labia majora or
lower vestibule.
• Whereas most cysts and abscesses lead to asymmetry of labial
anatomy, some smaller cysts may only be detected by palpation.
• Bartholin abscesses on the verge of spontaneous decompression
will exhibit an area of softening where rupture will most likely
occur.
Treatment
• Small, asymptomatic cysts require no intervention except
to exclude neoplasia in women older than 40 years.
• Multiple techniques exist for managing cysts that
cause significant pressure symptoms or become
infected.
• These include incision and drainage, marsupialization,
and Bartholin gland excision
Reference
• Schorge, Schaffer, Halvorson, Hoffman, Bradshaw,
Cunningham. Williams Gynecology. 1st ed. United States
of America: McGraw Hill; 2008.
Abses
Etiolog
y
• MSSA, MRSA. Much less commonly, other organisms.
• Sterile abscess can occur as a foreign-body response
(splinter, ruptured inclusion cyst, injection sites).
• Cutaneous odontogenic sinus can appear anywhere on
the lower face, even at sites distant from the origin
Predisposing
Factors
• Chronic S. aureus carrier state (nares, axillae,
perineum, vagina)
• Diabetes mellitus
• Obesity
• Poor hygiene
• Bactericidal defects (e.g., chronic granulomatous
disease)
• Chemotactic defects
PATHOGENE
SIS
• Folliculitis, furuncles, and carbuncles represent a continuum
of severity of S. aureus infection.
• Portal of entry: hair follicle, break in the integrity of skin.
• MRSA infections often have high morbidity due to delay
in administration of effective antibiotic.
• Control/eradication of carrier state treats/prevents
folliculitis, furuncle, and carbuncle formation.
CLINICAL
MANIFESTATION
• Duration of Lesions Days to weeks to months.
• Skin Symptoms Throbbing pain. Tenderness
• Constitutional Symptoms Carbuncles may be accompanied
by low-grade fever and malaise.
• Skin Lesions Lesions are red, hot, and painful/ tender.
• Abscess
• May arise in any organ or structure.
• Abscesses that present on the skin arise in the dermis, subcutaneous
fat, muscle, or a variety of deeper structures.
• Initially, a tender red nodule forms.
• In time (days to weeks), pus collects within a central space.
• A well-formed abscess is characterized by fluctuance of the central
portion of the lesion and can occur at any cutaneous site.
• At sites of trauma.
• Upper back for abscesses in ruptured inclusion cysts. Single or multiple.
Furuncl
e
• Initially, a firm tender nodule, up to 1–2 cm in diameter
• In many individuals, furuncles occur in setting of
staphylococcal folliculitis in beard area or neck.
• Nodule becomes fluctuant, with abscess formation ±
central pustule.
• Nodule with cavitation remains after drainage of abscess.
• A variable zone of cellulitis may surround the furuncle.
• Distribution: any hair-bearing region: beard area, posterior
neck and occipital scalp, axillae, buttocks.
• Single or multiple
Carbuncl
e
• Evolution is similar to that of furuncle.
• Composed of several to multiple, adjacent,
coalescing furuncles
• Characterized by multiple loculated dermal and
subcutaneous abscesses, superficial pustules, necrotic plugs,
and sieve-like openings draining pus
DIFFERENTIAL
DIAGNOSIS
• Painful Dermal/Subcutaneous Nodule
• Ruptured epidermoid or pilar cyst, hidradenitis
suppurativa (axillae, groin, vulva), necrotizing
lymphangitis.
LABORATORY
EXAMINATIONS
• Gram Stain Gram-positive cocci within
polymorphonuclear (PMN) leukocytes.
• Bacterial Culture Culture of pus isolates S. aureus .
Sensitivities to antimicrobial agents may determine
management.
• Antibiotic Sensitivities Identifies MRSA and need for
changing usual antibiotic therapy
Dermatopatholog
y
• Pyogenic infection arising in hair follicle and extending
into deep dermis and subcutaneous tissue (furuncle) and
with loculated abscesses (carbuncle).
MANAGEMEN
T
• The treatment of an abscess, furuncle, or carbuncle is incision
and drainage plus systemic antimicrobial therapy.
• Prevention Mupirocin ointment is effective for eliminating
nasal carriage.
• Surgery Incision and drainage are often adequate for treatment of
abscesses, furuncles, or carbuncles. Scissors or scalpel blade can
be used to drain loculated pus in carbuncles; if this is not done,
resolution of pain and infection can be delayed despite systemic
antibiotic therapy.
• Adjunctive Therapy Application of heat to the lesion
promotes localization/consolidation and aids early
spontaneous drainage.
• Systemic Antimicrobial Treatment Systemic antibiotics
speed resolution in healthy individuals and are mandatory
in any individual at risk for bacteremia (e.g.,
immunosuppressed patients).
Reference
• Wolff K, Allen Johnson R. Fitzpatrick’s Color Atlas & Synopsis
of
Clinical Dermatology. 6th ed. McGraw Hill; 2009.
Corpus Alineum Vagina
CORPUS ALIENUM pada VAGINA
• Pada penderita psikopatia seksualis
• Dampak benda asing tergantung bentuk dan jenis
benda
CORPUS ALIENUM pada VAGINA

Benda berbahan kain


• Infeksi dan leukorea berbau

Pesarium
• Iritasi dan perlukaan bila tidak dikeluarkan
dan dibersihkan berkala
Abortus Provocatus Kriminalis
• Tidak steril, atau traumatik
KISTA GARTNER (Gartner’s Duct Cyst)

Berasal dari sisa kanalis Wolfii (duktus


gartner)

Berjalan di sepanjang
permukaan anterior & bagian
atas vagina

Ukuran bervariasi tergantung ukuran


duktus dan kapasitas tampung cairan
di dalamnya
KISTA GARTNER (Gartner’s Duct Cyst)
• Lokasi di anterolateral puncak
vagina
Gambaran
• Gambaran
• Perabaan kistik, dilapisi
Klinikdinding translusen tipis epitel
kuboid/kolumner
Klinik • Dengan/tanpa silia, kadang
tersusun
stratified

• Terapi
• Insisi dinding anterolateral vagina
dan eksisi untuk mengeluarkan kista
Terapi dari sisa kanalis wolfii ini
KISTA NABOTHI (Kista Retensi)

Epitel kelenjar endoserviks :


kolumnar tinggi yang rentan infeksi /
epidermidisasi skuamosa

Metaplasia skuamosa yang


menyebabkan penutupan
muara kelenjar endoserviks

Sekret tertahan dan


berkembang menjadi kantong
kista
KISTA NABOTHI (Kista Retensi)
• Pada inspekulo tampak
penonjolan kistik area
Gambaran endoserviks dengan batas
• Gambaran Kliniktegas dan berwarna lebih
Klinik merah muda dibanding
sekitar

• Terapi
• Tidak ada terapi khusus
untuk kista nabothi
Terapi
Daftar Pustaka
• Buku Ilmu Kandungan Edisi Ketiga, Sarwono
Prawirohardjo ; 2011
Kehamilan Ektopik
• Kehamilan ektopik  suatu kehamilan yg pertumbuhan sel telur yg telah dibuahi
tidak menempel pada dinding endometrium, >95% berada di tuba fallopii
• Patfis  sel telur yg telah di buahi perjalanan nya tersendat menuju
endometrium, shg embrio sdh berkembang sblm mencapai kavum uteri  akan
tjd perdarahan jk tempat nidasi tsbt tdk dpt menyesuaikan diri dg besarnya
perkembangan embrio
• Berdasarkan lokasi:
– Kehamilan tuba (>95%) tdri atas: pars ampularis (55%), pars ismika (25%), pars fimbrae
(17%)
– Kehamilan ektopik lain (<5%) antara lain di serviks, ovarium atau abdominal
– Kehamilan intraligamenter (sgt sdikit)
– Kehamilan heterotopik, mrpkan kehamilan ganda dmna satu janin berada di cavum uteri
dan yg lain mrpkan kehamilan ektopik
– Kehamilan ektopik bilateral
Etiologi
• Faktor yg menyebabkan hambatan nidasi embrio ke endometrium:
– Faktor tuba  infeksi tuba(lumen menyempit), pasca operasi rekanalisasi,
hipoplasia uterus, tuba yg berkelok dan silia yg tdk berfungsi baik,
endometriosis tuba, divertikel tuba kongenital, tumor (mioma uteri, tumor
ovarium)
– Faktor abnormalitas dari zigot  zigot tumbuh terlalu cepat/ terlalu besar
shg tersendat di tuba
– Faktor ovarium  ovum yg ditangkap oleh tuba yg kontralateral
– Faktor hormonal  progesteron menyebabkan gerakan tuba melambat
– Faktor lain  IUD, umur, perokok
Patologi
• Embrio yg tdk mencapai endometrium  tumbuh di tuba  akan mengalami bbrp hal:
– Hasil konsepsi mati dini dan di resorbsi  pd implantasi scra kolumner, ovum yg dibuahi cepat mati
akrena vaskularisasi kurang lalu diresorbsi total, pd keadaan ini penderita hnya mengalami
keterlambatan haid
– Abortus ke dalam lumen tuba (abortus tubaria)  akibat perdarahan pd dinding tuba tempat
implantasi shg embrio terlepas dan masuk ke ostium tuba pars abdominalis (sering pd kehamilan pars
ampularis), pd keadaan ini penderita mengalami perdarahan terus menerus lalu tuba membesar dan
kebiruan (hematosalping) lalu darah mengalir ke rongga perut melalui ostium tuba. Darah akan
terkumpul di kavum Douglasi dan membentuk hematokel retrouterina
– Ruptur dinding tuba  tjd bila ovum berimplantasi pada ismus (kehamilan muda) dan implantasi
pada pars interstisialis (kehamilan lanjut). Faktor utama penyebab ruptur adalah penembusan vili
korialis ke lap muskularis dan peritoneum. Tjd perdarahan dlm rongga perut, syok, kematian. Bila
psudokapsularis pecah , makan tjd perdarahan dalam lumen tuba
Gambaran Klinik
• Biasanya dokter dan penderita tdak mengetahui adanya kelainan smp tjdnya abortus atau ruptur tuba
• Pem vaginal, uterus membesar dan lembek, nyeri goyang +, cavum douglasi menonjol dan nyeri pd
perabaan, pd abortus tuba teraba tumor disamping uterus
• Pem bimanual tuba lembek dan sukar diraba
• Pem USG  uterus tdk ada kantong gestasi dan kantong gestasi berada di luar uterus, jk ruptur 
mk kantong gestasi terlihat hiperekoik dan tidak beraturan, tidak berbatas jelas, disekitarnya
terdapat cairan bebas, terdpt cairan eksudat (dihslkan sel desidua) yg terlihat sbg struktur cincin
anekoik yg disebut kantong gestasi palsu/ pseudogestational sac
• Jk tdk terdpt USG  kuldosentesis
• Jk kehamilan ektopik mngalami ruptur  sakit/nyeri perut mendadak, perdarahan, syok, pingsan
• Jk tjd abortus  nyeri perut, dpt menjalar ke perut tengah ataupun seluruh perut, nyeri bahu (akibat
darah pd rongga perut merangsang diafragma), defekasi nyeri (jk terbentuk hematokel retrouterina)
• Perdarahan pervaginam
• Amenorea
Pd kehamilan ektopik di pars ampula tuba yg blm
Diagnosis pecah bisa dicoba ditangani dengan kemoterapi
(digunakan metotreksat 1mg/kg IV dan faktor
sitrovorum 0,1 mg/kg IM berselang seling , selama 8
hari) untuk menghindari pembedahan dg syarat: –
kehamilan di pars ampula tuba belum pecah –
diameter kantong gestasi ≤4cm –perdarahan dlm
rongga perut ≤100ml –tanda vital baik dan stabil
Prognosis
• Kematian karena kehamilan ektopik terganggu cenderung
turun dg diagnosis dini dan persediaan darah yg cukup
• Akan ttpi jk pertolongan terlambat, maka angka kematian
dapat tinggi
Polip serviks
Polip serviks
• Microglandular hyperplasia (MGH) usually occurs in women
of reproductive age, but 6% of known cases are detected in
postmenopausal women.
• Essentials of Diagnosis
– Intermenstrual or postcoital bleeding.
– A soft, red pedunculated protrusion from the cervical canal at
the external os.
– Microscopic examination confirms the diagnosis of benign
polyp.
General Considerations
• Cervical polyps are small, pedunculated, often sessile neoplasms of the
cervix. Most originate from the endocervix; a few arise from the portio.
They are composed of a vascular connective tissue stroma and are
covered by columnar, squamocolumnar, or squamous epithelium.
• Polyps are common in multigravidas over 20 years of age.
• Cervical cancers present as a polypoid mass.
• Polyps is due to chronic inflammation, an abnormal local responsiveness
to hormonal stimulation, or a localized vascular congestion of cervical
blood vessels is not known. They are often found in association with
endometrial hyperplasia, hyperestrogenism plays a significant etiologic
role.
• Endocervical polyps usually are red, flame-shaped, fragile growths.
X-Ray Findings
• Polyps high in the endocervical canal may be demonstrated
by hysterosalpingogram or saline infusion
sonohysterography
Laboratory Findings
• Vaginal cytology will reveal signs of infection and often mildly atypical
cells. Blood and urine studies are not helpful.
Special Examination
• A polyp high in the endocervical canal may be seen with the aid of a
special endocervical speculum or by hysteroscopy. Some polyps are
found only at the time of diagnostic D&C in the investigation of
abnormal bleeding.
Treatment
Medical Measures
• Appropriate testing for cervical discharge should be performed
as indicated and treatment administered if infection is
identified.
Specific Measures
• Most polyps can be removed in office. Large polyps and those
with sessile attachments may require excision in an operating
room.
• All tissue must be sent to a pathologist to be examined for
possible underlying malignant or premalignant conditions.
Complications
• Cervical polyps may be infected, some by virulent staphylococci,
streptococci, or other pathogens. Serious infections occasionally
follow instrumentation for the identification or removal of polyps.
A broad-spectrum antibiotic should be administered at the first
sign or symptom of spreading infection.
• Acute salpingitis may be initiated or exacerbated by polypectomy.
• It is unwise to remove a large polyp and then perform a
hysterectomy several days thereafter. Pelvic peritonitis may
complicate the latter procedure. A delay of several weeks or 1
month between polypectomy and hysterectomy is
recommended.
Prognosis
• Simple removal of cervical polyps is usually
curative.
Reference
• DeCherney, AH, et al. Current Diagnosis & Treatment
Obstetrics & Gynecology.
Prolaps Uterus
Prolaps uterus
Causes:
• Anatomic findings
• Risk factors
– Age
– increasing parity
– Obesity
– history of pelvic surgery
– Lifestyle or disease
conditions: Chronic
coughing, chronic
constipation -- may
increase the pressures on
the pelvic floor.
Repetitive heavy lifting.
Symptoms
• Bulge Symptoms – the sensation or visualization of a vaginal or perineal
protrusion, and the sensation of pelvic pressure.
• Urinary Symptoms -- stress, urge urinary incontinence, frequency, urgency,
urinary
retention, recurrent UTI.
• Gastrointestinal Symptoms
– Constipation. Replacement of prolapse either by surgical repair or with a pessary does not
usually cure constipation.
– Anal incontinence of flatus or liquid or solid stool. Prolapse may lead to stool trapping in the
distal rectum with subsequent leakage of liquid stool around retained feces.
• Sexual Dysfunction
• Pelvic and Back Pain
• Mild to advanced prolapse-- asymptomatic.
Clinical Findings
• Examination should begin in the dorsal lithotomy position.
Vaginal support can then be assessed with strain (cough or
Valsalva) and the point of maximal protrusion should be
noted in centimeters relative to the hymen and recorded.
• A speculum also be used to evaluate uterocervical support.
• Imaging: sonography, computed tomography (CT),
and magnetic resonance imaging (MRI).
Prevention
• Antepartum and intrapartum and postpartum exercises,
especially those designed to strengthen the levator and perineal
muscle groups (Kegel), often help improve or maintain pelvic
support.
• Obesity, chronic cough, straining, and traumatic deliveries must
be corrected or avoided.
• Estrogen therapy following the menopause may help to
maintain the tone and vitality of pelvic musculofascial tissues
and thereby prevent or postpone the appearance of anterior
vaginal prolapse and other forms of relaxation.
Treatment
1. Conservative
• Pessary. Provide adequate
relief of symptoms, for the
patient with complicating
medical factors who is a
poor operative risk.
Prolonged use of pessaries,
may lead to pressure
necrosis and vaginal
ulceration.
Treatment
• Kegel exercises.
To tighten and strengthen the pubococcygeus muscles. Evidence
strongly supports use of Kegel exercises as first-line management
in the treatment of urinary and fecal incontinence.
• Estrogens.
In postmenopausal women, local estrogen therapy for a number
of months may improve the tone, quality, and vascularity of the
musculofascial supports.

2. Surgery
Reference
• Schorge JO, et.al. 2008. Williams Gynecology. The McGraw-
Hill Companies.
• DeCherney, AH, et.al. Current Diagnosis & Treatment
Obstetrics & Gynecology.
POLYCYSTIC OVARIAN
SYNDROME
Definition
• Women with polycystic ovarian syndrome (PCOS) have
abnormalities in the metabolism of androgens and estrogen
and in the control of androgen production. PCOS can result
from abnormal function of the hypothalamic-pituitary-
ovarian (HPO) axis. A woman is diagnosed with polycystic
ovaries (as opposed to PCOS) if she has 12 or more follicles
in at least 1 ovary.
Etiology
• Women with polycystic ovarian syndrome (PCOS) have abnormalities in the metabolism
of androgens and estrogen and in the control of androgen production. High serum
concentrations of androgenic hormones, such as testosterone, androstenedione, and
dehydroepiandrosterone sulfate (DHEA-S), may be encountered in these patients.
• PCOS is also associated with peripheral insulin resistance and hyperinsulinemia,
and obesity amplifies the degree of both abnormalities. Insulin resistance in PCOS can
be secondary to a postbinding defect in insulin receptor signaling pathways, and
elevated insulin levels may have gonadotropin-augmenting effects on ovarian
function.
Hyperinsulinemia may also result in suppression of hepatic generation of sex
hormone–
binding globulin (SHBG), which in turn may increase androgenicity.
• Insulin resistance in PCOS has been associated with adiponectin, a hormone secreted by
adipocytes that regulates lipid metabolism and glucose levels. Lean and obese women
with PCOS have lower adiponectin levels than do women without PCOS.
Pathology Anatomy
• In polycystic ovarian syndrome (PCOS), histologic changes of the
ovary include enlarged, sclerotic, multiple cystic follicles (see the
image below). As previously stated, a woman is diagnosed with
polycystic ovaries (as opposed to PCOS) if she has 12 or more
follicles in at least 1 ovary, measuring 2-9 mm in diameter, or a
total ovarian volume greater than 10 cm3.
Sign and Symptoms
• The major features of PCOS include menstrual
dysfunction, anovulation, and signs of hyperandrogenism.
• Other signs and symptoms of PCOS may include the
following:
– Hirsutism
– Infertility
– Obesity and metabolic syndrome
– Diabetes
– Obstructive sleep apnea
History & Physical Examination
• The family history of patients with polycystic ovarian syndrome (PCOS)
may include the following:
– Menstrual disorders
– Adrenal enzyme deficiencies
– Hirsutism
– Infertility
– Obesity and metabolic syndrome
– Diabetes
• On examination, findings in women with PCOS may include the following:
– Virilizing signs
– Acanthosis nigricans
– Hypertension
– Enlarged ovaries: May or may not be present; evaluate for an ovarian mass
Furthered Diagnoses
• Testing
– Exclude all other disorders that can result in menstrual irregularity and
hyperandrogenism, including adrenal or ovarian tumors, thyroid dysfunction,
congenital adrenal hyperplasia, hyperprolactinemia, acromegaly, and
Cushing syndrome.
– Baseline screening laboratory studies for women suspected of having PCOS
may include the following:
• Thyroid function tests (eg, TSH, free thyroxine)
• Serum prolactin level
• Total and free testosterone levels
• Free androgen index
• Serum hCG level
• Cosyntropin stimulation test
• Serum 17-hydroxyprogesterone (17-OHPG) level
• Urinary free cortisol (UFC) and creatinine levels
• Low-dose dexamethasone suppression test
• Serum insulin-like growth factor (IGF)–1 level
– Other tests used in the evaluation of PCOS include the following:
• Androstenedione level
• FSH and LH levels
• GnRH stimulation testing
• Glucose level
• Insulin level
• Lipid panel
Furthered Diagnoses
• Imaging tests
– The following imaging studies may be used in
the evaluation of PCOS:
– Ovarian ultrasonography, preferably using
transvaginal approach
– Pelvic CT scan or MRI to visualize the adrenals
and ovaries
• Procedures
– An ovarian biopsy may be performed for histologic
confirmation of PCOS; however, ultrasonographic
diagnosis of PCOS has generally superseded
histopathologic diagnosis. An endometrial biopsy
may be obtained to evaluate for endometrial
disease, such as malignancy.
Differential Diagnoses
• Although no agreed-upon diagnostic criteria currently exist for
adolescent polycystic ovarian syndrome (PCOS), hyperandrogenemia
is essential for the diagnosis in this age group.
• All conditions that mimic PCOS should be ruled out before a diagnosis
of PCOS is confirmed. Consider the following in the differential
diagnosis of PCOS:
– Ovarian hyperthecosis
– Congenital adrenal hyperplasia (late-onset)
– Drugs (eg, danazol, androgenic progestins)
– Hypothyroidism
– Patients with menstrual disturbances and signs of hyperandrogenism
– Idiopathic hirsutism
– Familial hirsutism
– Masculinizing tumors of the adrenal gland or ovary (rapid onset of signs of
virilization)
– Cushing syndrome (low K+, striae, central obesity, high cortisol; high
androgens in adrenal carcinoma)
– Hyperprolactinemia
– Exogenous anabolic steroid use
– Stromal hyperthecosis (valproic acid)
OVARIAN
TORSION
Definition
• Ovarian torsion (adnexal torsion) is an infrequent but significant
cause of acute lower abdominal pain in women. This condition is
usually associated with reduced venous return from the ovary as
a result of stromal edema, internal hemorrhage,
hyperstimulation, or a mass. The ovary and fallopian tube are
typically involved.
• The clinical presentation is often nonspecific with few distinctive
physical findings, commonly resulting in delay in diagnosis and
surgical management. A quick and confident diagnosis is
required to save the adnexal structures from infarction.
Etiology
• Anatomic changes affecting the weight and the size of the ovary may alter the position of
the fallopian tube and allow twisting to occur.
• Pregnancy is associated with, and may be responsible for, torsion in approximately 20% of
adnexal torsion cases, [1] probably secondary to the ovarian enlargement that occurs
during ovulation in combination with laxity of the supporting tissues of the ovary.
• Congenitally malformed and elongated fallopian tubes may be seen, particularly in young,
prepubertal patients.
• Ovarian tumors, both benign and malignant, are implicated in 50-60% of cases of
torsion. Involved masses are nearly all larger than 4-6 cm, although torsion is still
possible with smaller masses. Dermoid tumors are most common. Malignant tumors
are much less likely to result in torsion than benign tumors are. This is because of the
presence of cancerous adhesions that fix the ovary to surrounding tissues.
• Conversely, patients with a history of pelvic surgery (principally tubal ligation) are at
increased risk for torsion, probably because of adhesions that provide a site around
which the ovarian pedicle may twist.
Pathophysiology
• Ovarian torsion involves torsion of the ovarian tissue on its pedicle leading
to reduced venous return, stromal edema, internal hemorrhage, and
infarction with the subsequent sequelae. Ovarian cysts are 3 times more
common in ovarian torsion cohorts than in the general population, and
evidence suggests that ovarian cysts are very common in asymptomatic
pregnant women but spontaneously resolve as the pregnancy progresses.
Pregnancy is a risk factor for torsion (odds ratio: 18:1) but remains an
uncommon event (0.167%).
• Ovarian torsion classically occurs unilaterally in a pathologically enlarged
ovary. The irregularity of the ovary likely creates a fulcrum around which the
oviduct revolves. The process can involve the ovary alone but more
commonly affects both the ovary and the oviduct (adnexal torsion).
Approximately 60% of cases of torsion occur on the right side.
• Although torsion may rarely occur in normal adnexa, it more frequently
arises from one of many anatomic changes. Torsion of a normal ovary is
most common among young children, in whom developmental abnormalities
(eg, excessively long fallopian tubes or absent mesosalpinx) may be
responsible. In fact, fewer than half of ovarian torsion cases in pediatric
patients involve cysts, teratomas, or other masses.
• During early pregnancy, the presence of an enlarged corpus luteum cyst
likely predisposes the ovary to torsion. Women undergoing induction of
ovulation for infertility carry an even greater risk, in that numerous theca
lutein cysts significantly expand the ovarian volume.
Sign and Symptoms
• Classically, patients present with the sudden onset (commonly during exercise
or other agitating movement) of severe, unilateral lower abdominal pain that
worsens intermittently over many hours. A minority of patients, however,
complain of mild pain that follows a more prolonged time course. The pain
usually is localized over the involved side, often radiating to the back, pelvis, or
thigh. Approximately 25% of patients experience bilateral lower quadrant pain.
It may be described as sharp and stabbing or, less frequently, crampy.
• Nausea and vomiting occur in approximately 70% of patients, mimicking
a gastrointestinal source of pain and further obscuring the diagnosis.
• A history of previous episodes may be elicited, possibly attributable to
partial, spontaneously resolving torsion. Fever may occur as a late finding as
the ovary becomes necrotic.
Physical Examination
• The physical examination, like the history, is typically nonspecific
and is highly variable. A unilateral, tender adnexal mass has been
reported in between 50 and 90% of patients. However, the
absence of such a finding does not exclude the diagnosis.
Tenderness to palpation is common; however, it is mild in
approximately 30% and absent in another 30% of patients.
Therefore, the absence of tenderness cannot be used to rule out
torsion.
• Peritoneal findings are infrequent and indicate advanced disease
if present.
Furthered Diagnoses
• Diagnostic ultrasonography should be the first
examination performed; typically, the affected ovary
is enlarged, with multiple immature or small follicles
along its periphery.
• Ultrasonography with color Doppler analysis is the
method of choice for the evaluation of adnexal
torsion because it can show morphologic and
physiologic changes in the ovary and can help in
determining whether blood flow is impaired. Gray-
scale and spectral findings are correlated with the
age of the torsion (ie, acute torsion or chronic
torsion) and the degree of the twist or torsion.
Normal Doppler imaging must not, however, be used
as a basis for excluding the diagnosis.
Furthered Diagnoses
• Rarely, computed tomography (CT) or
magnetic resonance imaging (MRI) is
needed to make a definitive diagnosis. CT
or MRI can serve as a secondary modality
when ultrasonographic findings are
nondiagnostic.
• Culdocentesis is a nonspecific test that is
unlikely to confirm or exclude torsion
and therefore is not recommended in
the diagnostic workup.
Differential Diagnoses
• Appendicitis
• Cystitis in Females
• Diverticulitis
• Ectopic Pregnancy
• Endometriosis
• Large-Bowel Obstruction
• Nephrolithiasis
• Ovarian Cysts
• Pelvic Inflammatory Disease
• Small-Bowel Obstruction
• Urinary Tract Infections in
Pregnancy
OVARIAN CYST
RUPTURE
Definition
• A ruptured ovarian cyst is a common phenomenon, with
presentation ranging from no symptoms to symptoms mimicking
an acute
abdomen. Sequelae vary. Menstruating women have rupture of a
follicular cyst every cycle, which is either asymptomatic or with mild
transient pain (mittelschmerz). In less usual circumstances, the rupture
can be associated with significant pain. In very rare circumstances,
intraperitoneal hemorrhage and death may occur.
• The most pressing issues facing clinicians encountering patients with
potential cyst rupture in the acute setting are to rule out ectopic
pregnancy, ensure adequate pain control, and rapidly assess the patient
for hemodynamic instability to allow appropriate triage. Although most
patients require only observation, some need analgesics for pain control
and laparoscopy or laparotomy for diagnosis or to achieve hemostasis.
Pathophysiology
• Each month, a mature ovarian follicle ruptures, releasing an ovum
so the process of fertilization can begin. Occasionally, these
follicles may bleed into the ovary, causing cortical stretch and
pain, or at the rupture site following ovulation. Similarly, a
corpus luteum cyst may bleed subsequent to ovulation or in early
pregnancy. As blood accumulates in the peritoneal cavity,
abdominal pain and signs of intravascular volume depletion may
arise.
• The etiology of this increased bleeding is unknown, although
abdominal trauma and anticoagulation treatments may increase
the risk. Nonphysiologic cysts, such as cystadenomas and mature
cystic teratomas (dermoid cysts), may, in rare cases, rupture and
cause symptoms. In addition to hemorrhage, significant pain can
accompany rupture of a dermoid cyst, presumably from spillage
of sebaceous fluid, resulting in a diffuse chemical peritonitis.
Sign and Symptoms
• The patient often presents with an acute onset of abdominal
pain, typically during strenuous physical activity, such as exercise
or sexual intercourse. Given that follicular cyst rupture is more
common than corpus luteal cyst rupture, the onset tends to be
midcycle. Other associated symptoms include the following:
– Vaginal bleeding
– Nausea and/or vomiting
– Weakness
– Syncope
– Shoulder tenderness
– Circulatory collapse
Physical Examination
• Vital signs are usually within normal range. Physical findings
can range from mild unilateral low abdominal tenderness to
those of an acute abdomen with severe tenderness,
guarding, rebound, and peritoneal signs.
• Low-grade fever is sometimes observed, and an adnexal mass
may be palpable, although absence of such findings on
examination has no diagnostic value as many cysts
decompress after rupture. Orthostatic changes are consistent
with a sizable hemorrhage.
Furthered Diagnoses
• Perform a urine pregnancy test. If the pregnancy test is
positive, make sure to rule out an ectopic pregnancy.
Evaluate for ovarian torsion before discharge. If a
diagnosis of bleeding ruptured ovarian cyst is considered,
make sure the hemoglobin level is stable before
discharging the patient. It is appropriate to admit the
patient for observation and pain control.
• Perform a diagnostic laparoscopy and/or laparotomy if
the patient is hemodynamically unstable or if a specific
diagnosis is unclear, yet a definitive diagnosis is
necessary.
• C-reactive protein (CRP) levels can be used
preoperatively to differentiate a ruptured ovarian cyst
from ovarian torsion.
• Plasma D-dimer levels may be markers for
endometriotic ovarian cyst rupture.
Furthered Diagnoses
• Serum or urine pregnancy testing should be performed.
In the case of a positive result, the patient should be
evaluated for ectopic pregnancy. If concerned regarding
possible hemorrhage, monitor the hematocrit (serially, if
necessary) to ensure there is no continued bleeding.
• If the diagnosis is unclear, urinalysis should be performed
to identify a possible urinary tract infection or renal or
bladder stones. Blood, urine, and cervical cultures may
also be indicated rule out pelvic inflammatory disease or
urinary tract infections.
• Blood type and cross-match are indicated in patients with
significant peritoneal signs or hemodynamic instability,
because such patients may require surgical intervention
or blood transfusion.
Furthered Diagnoses
• Ultrasonography is the preferred imaging modality for assessing
gynecologic structures, given its low cost, availability, and
sensitivity in recognizing adnexal cysts and hemoperitoneum.
Despite this, there remain instances in which the ultrasound
findings are nonspecific, particularly after rupture and
decompression of a cyst in the setting of apparent physiologic
levels of fluid in the pelvis.
• If ultrasound yields ambiguous results in a patient with significant
pain, computed tomography (CT) of the pelvis with contrast
should be performed. CT features of corpus luteum cysts have
been previously described.
• Although commonly performed in the past, culdocentesis has
been largely abandoned in favor of ultrasonography and CT
scanning, as both can readily identify fluid collections in the cul-
de-sac. Culdocentesis is still acceptable, however, in locations
where imaging is not available.
Differential Diagnoses
• Abdominal Trauma, Blunt
• Appendicitis
• Bladder Stones
• Cystitis, Nonbacterial
• Diverticulitis
• Ectopic Pregnancy
• Nephrolithiasis
• Ovarian Cysts
• Pelvic Inflammatory
Disease
References
• http://emedicine.medscape.com/article/256806-overview
• http://emedicine.medscape.com/article/2026938-overview
• http://emedicine.medscape.com/article/253620-overview
KISTA
OVARIUM
Klasifika
si
• Meliputi:
– Kistadenoma ovarii serosum
– Kistadenoma ovarii
musinosum
– Kista dermoid
Kistadenoma Ovarii
Serosum
• Epidemiologi:
– Mencakup sekitar 15-25% dari keseluruhan tumor jinak ovarium
– Usia penderita berkisar antara 20-50 tahun
– Pada 12-50% kasus, kista mengenai kedua ovarium (bilateral)
• Gambaran umum:
– Ukuran kista berkisar antara 5-15 cm, lebih kecil dari rata-rata
ukuran kistadenoma musinosum
– Kista berisi cairan serosa, jerning kekuningan
– Proliferasi fokal pada dinding kista menyebabkan proyeksi papilomatosa
ke tengah kista yang dapat bertransformasi menjadi kistadenoma
fibroma
• Gambaran klinik:
– Tidak dijumpai gejala klinik khusus yang
dapat menjadi petanda
– Pada sebagian besar kasus, tumor ini ditemukan
secara kebetulan saat dilakukan pemeriksaan
rutin
– Keluhan yang dapat timbul: rasa tidak nyaman
di pelvis, pembesaran perut, asites
• Diagnosis: Ditegakkan dengan pemeriksaan
USG
• Tatalaksana:
– Tindakan pembedahan: eksisi kista
– Pemeriksaan patologi anatomi
Kistadenoma Ovarii
Musinosum
• Epidemiologi:
– Mencakup sekitar 16-30% dari keseluruhan tumor jinak ovarium
– 85% kistadenoma ovarii musinosum adalah jinak
– Pada 5-7% kasus, kista mengenai kedua ovarium (bilateral)
• Gambaran umum:
– Terdiri dari beberapa jaringan penyusun tumor: ektodermal,
mesodermal, dan entodermal  ektodermal merupakan komponen
utama
– Mempunyai dinding berwarna putih dan relatif tebal, berisi cairan
kental dan berminyak karena dinding tumor mengandung banyak
kelenjar sebasea
• Gambaran klinik:
– Tidak dijumpai gejala klinik khusus yang dapat
menjadi petanda (asimptomatik)
– Keluhan yang dapat timbul: pertambahan berat badan,
rasa penuh di perut  tumor musin merupakan tumor
dengan ukuran terbesar dari tumor dalam tubuh
manusia (bisa lebih dari 70 kg)
– Pada perempuan pascamenopause dapat mengalami
hiperplasia endometrium  karena tumor
mengalami luteinisasi sehingga menghasilkan
hormon estrogen
• Diagnosis: Ditegakkan dengan pemeriksaan USG
• Tatalaksana:
– Tindakan pembedahan: salfingo-ooforektomi
unilateral
– Suction cairan musin dari kavum peritoneum
Kista
Dermoid
• Epidemiologi:
– Tumor terbanyak (10% dari total tumor ovarium) yang berasal dari
sel germinativum
– Paling banyak diderita oleh gadis yang berusia dibawah 20 tahun
• Gambaran umum:
– Tumor ini adalah tumor multilokuler
– Lokulus berisi cairan musinosum yang tampak berwarna kebiruan di
dalam kapsul yang dindingnya tegang
– Dinding tumor tersusun dari epitel kolumnar tinggi dengan inti
sel berwarna gelap terletak di bagian basal
• Gambaran klinik:
– Dalam ukuran kecil, kista dermoid
tidak menimbulkan keluhan apa pun
– Penemuan tumor pada umumnya
melalui pemeriksaan ginekologi rutin
– Bila ukuran tumor cukup besar: rasa penuh
dan berat di dalam perut
• Diagnosis: Ditegakkan dengan
pemeriksaan USG
• Tatalaksana:
– Tindakan pembedahan: laparotomi dan
kistektomi
Referens
i
• Anwar M, Baziad A, Prabowo P. Ilmu Kandungan. 3rd ed.
Jakarta: PT Bina Pustaka Sarwono Prawirohardjo;
2011.
Cervical cancer
Cervical cancer
•Recognition of the etiologic role of human papillomavirus (HPV)
infection in cervical cancer has led to the recommendation of adding
HPV testing to the screening regimen in women 30-65 years of age.
However, women who have symptoms, abnormal screening test results,
or a gross lesion of the cervix are best evaluated with colposcopy and
biopsy.

http://emedicine.medscape.com/article/253513-overview#a2
Cervical cancer
Human papillomavirus (HPV) infection must be present
for cervical cancer to occur. HPV infection occurs in a
high percentage of sexually active women.
However, approximately 90% of HPV infections clear on their
own within months to a few years and with no sequelae,
although cytology reports in the 2 years following infection
may show a low-grade squamous intraepithelial lesion.

http://emedicine.medscape.com/article/253513-overview#a3
Cervical cancer
On average, only 5% of HPV infections will result in the
development of CIN grade 2 or 3 lesions (the recognized
cervical cancer precursor) within 3 years of infection.
Only 20% of CIN 3 lesions progress to invasive cervical cancer
within 5 years
Only 40% of CIN 3 lesions progress to invasive cervical cancer
within 30 years.

http://emedicine.medscape.com/article/253513-overview#a3
Cervical cancer: CIN
Cervical intraepithelial neoplasia (CIN) arises in an area of
metaplasia in the transformation zone at the advancing
squamocolumnar junction (SCJ) in most cases. Metaplasia
advances from the original SCJ inward, toward the external os
and over the columnar villi, which establishes an area called
the transformation zone. CIN is most likely to begin either
during menarche or after pregnancy, when metaplasia is
most active; after menopause, metaplasia is less active and
a woman has a lower risk of developing CIN.
Berek & Novak’s Gynecology, 14th edition, 2007
Cervical cancer: CIN
Most CIN 1 (and some CIN 2) lesions regress spontaneously if
untreated; nevertheless, CIN refers to a lesion that may
progress to invasive carcinoma. This term is equivalent to the
term dysplasia,which means abnormal maturation;
consequently, proliferating metaplasia without mitotic
activity should not be called dysplasia.
Squamous metaplasia should not be diagnosed as dysplasia
(or CIN) because it does not progress to invasive cancer.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: CIN
• Approximately 90% of intraepithelial neoplasia is attributed to
human papillomavirus (HPV) infection. Only certain types of
HPV cause highgrade intraepithelial lesions and cancer (HPV- 16, -18,
-31, -33, -35, -39, -45, -51, -52, -56, and -58). Type 16
• is the most common form of HPV found in invasive cancer and
in CIN 2 and CIN 3; it is found in 47% of women with cancer in these
stages.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: Signs and symptoms
Vaginal bleeding is the most common symptom occurring in
patients with cancer of the cervix. Most often, this is
postcoital bleeding, but it may occur as irregular or
postmenopausal bleeding as well. Patients with advanced
disease may present with amalodorous vaginal discharge,
weight loss, or obstructive uropathy. In asymptomatic
women, cervical cancer is most commonly identified through
evaluation of abnormal cytologic screening tests.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: Signs and Symptoms
•The tumor grows by extending along the epithelial surfaces, both squamous and
glandular, upward to the endometrial cavity, throughout the vaginal epithelium, and
laterally to the pelvic wall. It can invade the bladder and rectum directly, leading to
constipation, hematuria, fistula, and ureteral obstruction, with or without
hydroureter or hydronephrosis.
•The triad of leg edema, pain, and hydronephrosis suggests pelvic wall
involvement. The common sites for distant metastasis include extrapelvic lymph
nodes, liver, lung, and bone.

http://emedicine.medscape.com/article/253513-clinical#b2
Cervical cancer: Physical Exam
•In patients with early-stage cervical cancer, physical examination
findings can be relatively normal. As the disease progresses, the cervix
may become abnormal in appearance, with gross erosion, ulcer, or
mass. These abnormalities can extend to the vagina.
•Rectal examination may reveal an external mass or gross blood from
tumor erosion.

http://emedicine.medscape.com/article/253513-clinical#b3
Cervical cancer: Physical Exam
•Bimanual pelvic examination findings often reveal pelvic or
parametrial metastasis. If the disease involves the liver,
hepatomegaly may develop. Pulmonary metastasis usually is difficult to
detect on physical examination unless pleural effusion or bronchial
obstruction becomes apparent. Leg edema suggests lymphatic or
vascular obstruction caused by tumor.

http://emedicine.medscape.com/article/253513-clinical#b3
Cervical cancer: Colposcopy
When obvious tumor growth is present, a cervical biopsy is
usually sufficient for diagnosis. If gross disease is not present,
a colposcopic examination with cervical biopsies and
endocervical curettage is warranted. If the diagnosis cannot
be established conclusively with colposcopy and directed
biopsies, cervical conization may be necessary.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: Colposcopy
Colposcopic examination is mandatory for patients
with suspected early invasive cancer based on cervical
cytology and a grossly normal-appearing cervix.
Colposcopic findings that suggest invasion are
– abnormal blood vessels,
– irregular surface contour with loss of surface epithelium,
and
– color tone change.
Colposcopically directed biopsies may permit the
diagnosis of frank invasion and thus avoid the need
for diagnostic cone biopsy, allowing treatment to be
administered without delay.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: pathology
Squamous cell carcinoma
Invasive squamous cell carcinoma is the
most common variety of invasive cancer
in the cervix.
Histologically, variants of squamous cell
carcinoma include large cell keratinizing,
large cell nonkeratinizing, and small cell
types

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: pathology
Adenocarcinoma
In recent years, there has been an increasing number of
cervical adenocarcinomas reported in women in their
20s and 30s. Although the total number of cases of
adenocarcinoma has been relatively stable, this
disease is being seen with increasing frequency in
young women, especially as the number of cases of
invasive squamous cell carcinoma decreases.
Adenocarcinoma of the cervix is managed in the
same a manner to that used for squamous cell
carcinoma.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: pathology
Adenocarcinoma
In recent years, there has been an increasing number of
cervical adenocarcinomas reported in women in their
20s and 30s. Although the total number of cases of
adenocarcinoma has been relatively stable, this
disease is being seen with increasing frequency in
young women, especially as the number of cases of
invasive squamous cell carcinoma decreases.
Adenocarcinoma of the cervix is managed in the
same a manner to that used for squamous cell
carcinoma.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: patterns of spread
Cancer of the cervix spreads by
• (i) direct invasion into the cervical stroma,
corpus, vagina, and parametrium;
• (ii) lymphatic metastasis;
• (iii) blood-borne metastasis; and
• (iv) intraperitoneal implantation.
The cervix is commonly involved in cancer of the
endometrium and vagina. The latter is rare,
and most lesions that involve the cervix and
vagina are designated cervical primaries

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: treatment by stage
Stage Ia
A microinvasive lesion is one in which
neoplastic epithelium invades the stroma to
a depth of less than 3 mm beneath the
basement membrane and in which lymphatic
or blood vascular involvement is not
demonstrated.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: treatment by stage
Stage Ia
Diagnosis must be determined on the basis of a
cone biopsy of the cervix. The treatment decision
rests with the gynecologist and should be
determined based on a review of the conization
specimen with the pathologist. It is important that
the pathologic condition be described in terms of (i)
depth of invasion,
(ii) width and breadth of the invasive area, (iii)
presence or absence of lymph—vascular space
invasion, and (iv) margin status. These variables
are used to determine the degree of radicality of
the operation and whether the regional lymph
nodes should be treated

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: treatment by stage
Stage Ia ≤3 mm Invasion
•Lesions with invasion less than or equal to 3
mm have less than 1% incidence of pelvic node
metastases.
•Treatment of microinvasive cervical
adenocarcinoma has been complicated by a
lack of agreement on approaches.
•Patients diagnosed with microinvasive
cervical adenocarcinoma should have expert
pathologic assessment before considering
treatment with extrafascial hysterectomy or
conization.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: treatment by stage
Stage Ia 3-5 mm Invasion
•Lesions with invasion of >3 to 5 mm have a
3% to 8% incidence of pelvic node
metastases

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: treatment by stage
Stage Ib1 and Ib2 Invasive Cancer
Stage Ib lesions are subdivided into stage
•Ib1, which denotes lesions that are 4 cm
or smaller in maximum diameter, and
stage
•Ib2, which denotes lesions that are larger
than 4 cm. These patients may be managed
with either radical trachelectomy or a type
III radical hysterectomy, with pelvic
lymphadenectomy.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: treatment by stage
Stage Ib1 and Ib2 Invasive Cancer
•Radical trachelectomy should be restricted to
candidates with low-risk disease, an absence of
lymph—vascular space invasion, and tumor size
less than 2 cm.
•The para-aortic lymph node chain must be evaluated,
especially if pelvic nodal disease is encountered.
Adjuvant radiation therapy is recommended if
intermediate-risk factors are identified
postoperatively. Adjuvant chemoradiation is indicated
if high-risk features are found.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: treatment by stage
Bulky Stage Ib2 and IIa Invasive Cancer
•Patients with bulky Ib2 and IIa disease may be
treated with either primary chemoradiation or
radical surgery. Because many of these patients will
be found to have intermediate- or high-risk factors
postoperatively, strong consideration should be given
to primary chemoradiation. If surgical therapy is
desired, a type III radical hysterectomy with pelvic
and para-aortic lymphadenectomy, followed by
adjuvant chemoradiation if intermediate- or high-risk
factors are present, is appropriate therapy.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: treatment by stage
Stage IIb to IIIb Invasive Cancer
•Therapy for patients with stage IIb or greater
cervical cancer has traditionally been
radiation therapy.
•Because chemoradiation has been shown
to be superior to radiation therapy alone,
chemoradiation is now the preferred
treatment strategy for these patients, with
cisplatin the chemotherapy agent of choice.

Berek & Novak’s Gynecology, 14th edition, 2007


Cervical cancer: treatment by stage
• Stage IVa and IVb Cancer
• Patients with stage IVb cervical carcinoma
are candidates for chemotherapy and
palliative pelvic radiation therapy. Control of
symptoms with the least morbidity is of
primary concern in this patient population.

Berek & Novak’s Gynecology, 14th edition, 2007


Ca Endometrium
Ca Endometrium

2/100.000 perempuan < 40 tahun

40-50/100.000 perempuan dekade 6-8

Kelanjutan lesi prakanker neoplasia intraepitel endometrium


5 years survival rate

Stadium Rate (%)


I 86
II 66
III 44
IV 16
Faktor Resiko
• Obesitas
• Rangsangan esterogen secara terus
menerus
• Menopause terlambat (lebih dari 52 tahun)
• Nulipara
• Siklus anovulasi
• Obat Tamoxifen
Gejala & Tanda
• Perdarahan uterus abnormal berupa metroragia /
perdarahan pascamenopause dan / atau keputihan
Diagnosis
• Biopsi endometrium / kuretase diagnostik
• Sigmoidoskopi / barium enema bila massa tumor di luar
uterus dengan simptoms saluran cerna
• CT Scan untuk identifikasi lokasi primer kanker
Daftar Pustaka
• Buku Ilmu Kandungan Edisi Ketiga, Sarwono
Prawirohardjo ; 2011
Koriokarsinoma
• Koriokarsinoma merupakan tumor ganas yang terdiri dari lapisan-lapisan
sel sitotrofoblas dan sinsitiotrofoblas dengan perdarahan, nekrosis, dan
invasi pembuluh darah yang jelas.
• Tumor ini digolongkan sebagai karsinoma epitel korionik tetapi
pola pertumbuhan dan metastasinya bersifat seperti sarkoma.
• Metastasis seringkali terjadi pada tahap dini dan hematogen karena afinitas
sel- sel trofoblas terhadap pembuluh darah.
• Tempat metastasis paling sering adalah paru-paru (sekitar 75%) dan
vagina (sekitar 50%).
• Kista teka lutein ovarium dapat ditemukanpada sepertiga kasus.
• Metastasis pada paru-paru memberikan empat gambaran khas: pola alveoler
atau "badai salju", densitas bulat, efusi pleura, serta emboli akibat oklusi
arteri pulmoner dan dapat menyebabkan hipertensi pulmoner
Kriteria diagnosis neoplasia trofoblastik
gestasional pascamolahidatidosa berdasarkan
FIGO Council 2000
• Peningkatan kadar hCG > 10"k pada tiga kali
pemeriksaan dalam waktu 2 minggu (hari 1, 7, dan 14).
• Kadar hCG menetap (t 10%) pada empat kali pemeriksaan
yang dilakukan dalam waktu 3 minggu (hari 1, 7, 14, dan 21,).
• Kadar hCG menetap dalam waktu > 6 bula pascaevakuasi
mola.
• Diagnosis histologi koriokarsinoma.
• Pasien dengan neoplasia trofoblastik gestasional menetap
ditangani di pusat rujukan dengan kemoterapi yang sesuai
(RCOG: III - sangat direkomendasikan berdasarkan
pengalaman klinik dari kelompok pembuat pedornan).
• Pasien risiko rendah, baik dengan penyakit metasrasis
maupun non-metastasis ditangani dengan pemberian
kemoterapi tunggal: merotreksat atau daktinomisin (II-3B).
• Pasien dengan risiko sedang diberi kemoterapi ganda dengan
MAC (metotreksat, daktinomisin, siklofosfamid, atau
klorambusil) atau EMA (etoposid, metotreksat, daktinomisin)
(SOGC: III-C); juga dapat digunakan kemoterapi tunggal (III-
C).
• Pasien risiko tinggi diberikan kemoterapi ganda, EMA/CO
(etoposid, metotreksat, daktinomisin diberikan interval satu
minggu diselingi dengan vinkristin dan siklofosfamid),
disertai pembedahan dan radioterapi selektif (SOCC: II-3B).
• Pada keadaan resisten, maka diberikan tindakan
penyelamatan berupa kemoterapi dengan EP/EMA (etoposid,
sisplatin, etoposid, metotreksat, daktinomisin) dan
pembedahan (SOGC: III-C).
• Pascakemoterapi, pasien tidak dianjurkan hamil hingga
kadar hCG normal selama 1 tahun (SOGC: III-C).
• Pil kontrasepsi kombinasi aman digunakan bagi
perempuan dengan neoplasia trofoblastik gestasional
(SOGC: III-C;.2
Daftar Pustaka
• Anwar M, Baziad A, Prabowo P. Ilmu Kandungan. 3rd ed.
Jakarta: PT Bina Pustaka Sarwono Prawirohardjo; 2011.
UTERINE FIBROIDS
(LEIOMYOMATAS)
What are
they?
• Smooth Muscle Tumor of the Uterus
• The most common uterine tumor
– Occurring in about 30% of women above the age of
30 years.
• Occurs up to 75% of hysterectomy specimens
• Symptomatic in 1/3 of cases
Patient
• Age: Characteristics
– 30-40 years.
– Rare before 30 or after 40 years
• Parity:
– Common in nulliparas, patients with low parity.
– It is rare in multiparas.
• Race:
– 3-9 times more common in negroids.
• Family history:
– Usually positive.
• Hyper-estrenemia:
– Estrogen receptors (ER) more than the surrounding myometrium but
less
than those in the endometrium
• Common in low parity.
• Atrophies and shrinks after menopause.
• Common association with other hyper-estrenic conditions as endometriosis,
endometrial hyperplasia and endometrial carcinoma.
Fibroid
s

Uterine Extrauterine
[99%] [1%]

Corporeal Cervical Genita Extragenit


[95%] [4%] l al

Interstitial Parasitic
[60%] Fibroid

Submucous Other
[ 20%] s

Subserous
[15%]
Characteristics
• Size
– from microscopic to very huge size filling the whole abdominal cavity (up to 40 kg
was recorded).
• Shape
– Spherical, flattened, or pointed according to the type.
• Cut section:
– On cut section,, whorly in appearance, and more pale than the surrounding uterine
muscle.
• Consistency:
– firmer than the surrounding myometrium.
– Soft fibroid occurs in pregnancy, cystic changes, vascular, inflammatory, and malignant
changes.
– Hard fibroid occurs in calcification.
• Capsule:
– Is a pseudo-capsule formed by compressed normal surrounding muscle fibres.
– the blood supply comes through it,
– it is the plain of cleavage during myomectomy
– its presence differentiate the myoma from adenomyosis.
• Blood supply:
– Nourishes the myoma from the periphery,
– The tumor itself is relatively avascular.
Presentations
• Asymptomatic:
– Accidentally discovered during examination.
– It is the commonest presentation, especially in subserous and interstitial fibroids.
• Vaginal bleeding: It is the commonest symptom,
– Menorrhagia or polymenorrhea: (commonest): This occurs due to:
• Associated hormonal imbalance and endometrial hyperplasia.
• Surface ulceration of submucous fibroid.
• Interstitial fibroid acts as F.B. preventing full contraction of myometrium to decrease
blood
loss.
• Pelvic congestion.
• Increased uterine size, vascularity, and endometrial surface area.
– Metrorrhagia: due to:
• In submucous fibroid due to ulceration of the surface, necrosis of the tip, or
secondary infection.
• Associated endometrial polyp.
• Associated malignancy (cancer body or sarcomatous change).
– Contact bleeding: (rare)
• ulcerated or infected tip of submucous fibroid polyp.
– Post-menopausal bleeding:
• Either due to sarcomatous change or associated endometrial carcinoma.
• Picture of iron deficiency anemia.
Presentations
• Discharge:
– Leucorrhea and mucoid discharge due to pelvic congestion.
– Muco-sanguinous discharge with ulcerated fibroid polyp.
– Muco-purulent discharge due to secondary infection.
• Swelling:
– Either abdominal swelling due to large fibroid or vaginal swelling due to a polyp.
• Infertility [in 5-10% of cases]:
– Most important is the underlying predisposing factor as anovulation and
hormonal
disturbance.
– Broad ligamentary fibroid may stretch or distort the tubes.
– Corneal fibroids may obstruct the uterine end of the tube.
– S.M.F. acts as F.B. interfering with implantation.
– Cervical fibroid may obstruct the cervical canal.
– Associated endometriosis or endometrial hyperplasia.
• Pain: uncommon
– Intermittent colicky pain in submucous fibroid (acts as F.B. in the uterine cavity).
– Dull-aching pain and congestive dysmenorrhea due to pelvic congestion.
– Acute abdomen in red degeneration, torsion, ruptured vessel, and inflammation.
Presentations
• Pressure symptoms
– Cervical fibroid:
• Anteriorly on the urethra causing acute retention of urine,
or
the bladder causing frequency of micturition.
• Laterally on the ureters causing colic and back pressure on
the
kidneys.
• Posteriorly on the rectum causing dyskasia, constipation,
and sense of incomplete defecation.
– Huge fibroid:
• On the pelvic veins causing edema, pain, and varicose veins
in
the lower limbs.
• On the GIT causing distension and dyspepsia.
• On the diaphragm causing dyspnea.
• Spontaneous abortion:
Signs of
fibroid
• General examination:
– signs of chronic anemia.
• Abdominal examination:
– large pelvi-abdominal swelling in huge fibroids.
• Pelvic examination:
– symmetrically or asymmetrically enlarged
uterus.
• Speculum examination
– fibroid polyp.
Differential
• Diagnosis
Causes of symmetrically enlarged uterus:
– Pregnancy
– Subinvolution of the uterus.
– Submucous or interstitial fibroid.
– Metropathia hemorrhagica.
– Adenomyosis uteri.
– Carcinoma or sarcoma of the uterus.
– Pyo, hemato, or physometra.
• Causes of asymmetrically enlarged
uterus:
– Subserous fibroid.
– Localized adenomyosis.
– Ovarian, tubal, or broad ligamentary
swelling.
Management
• Conservative Management
– small asymptomatic fibroid,
– fibroid in pregnancy or puerperium.
• Just keep observation every 6 months.
• Beware of underlying and/or
associated pathology
Medical
Treatment:
• Pre-operative till the time of surgery.
• Patient near the menopause, or newly
married with minimal symptoms.
• Red degeneration with pregnancy.
• Lines of treatment:
– Symptomatic:
• Correction of anemia,
• haemostatics,
• analgesics, and anti-spasmodics (anti-PG).
– Anti-estrogens:
• large dose of progesterone,
• Tamoxifen, Danazol,
• LH-RH analogues
– useful in decreasing the size and vascularity of the tumor by
50%
which is beneficial before myomectomy
Surgical Management
Myomectomy vs. Hysterectomy
??!!
• Indications:
• Symptomatic cases or uterus larger than 12
weeks size.
• Suspected malignancy (rapidly enlarging or post-
menopausal growth).
• Multiple huge fibroids liable to complications.
• Infertility.
Myomectomy
• Abdominal Myomectomy
• Vaginal Myomectomy
• Endoscopic Myomectomy
– Hysteroscopic
– Laparoscopic
• Embolization techniques
( Interventional Radiology)
Principle
• Myomectomy aims at
– removal of all the myomas,
– with conservation of a functioning uterus to
preserve the reproductive function.
• Generally the morbidity is higher than those
with hysterectomy.
– It is associated with much blood loss
– Liability of recurrence of fibroid.
• Myomectomy is better reserved only for
those keen to preserve the reproductive
function.
Principle
• The patient must be prepared for the possible need for
an emergency hysterectomy.
• Precautions to minimize blood loss during myomectomy:
– The timing of operation is post-menstrual (minimal pelvic
congestion).
– Pre-operative LH-RH analogues: may be given for 3 months
before surgery
to reduce the size and vascularity of the myomas.
– Intraoperative hemostasis
• Vertical midline incision is the least vascular
• application of Bonney’s myomectomy clamp or a rubber
tourniquet
• Use ring forceps to occlude the ovarian vessels
• Careful dissection to enucleate all the masses is needed to
avoid
recurrence.
• Avoid anesthetic agents that induce uterine relaxation (e.g.
halothane).
• Vasopressin (pitressin) 20 IU in 20 ml in normal saline are injected in
the uterine wall at the site of incision.
• Obliteration of the tumour cavities.
• Technique of abdominal myomectomy:
• Preliminary diagnostic curettage to exclude endometrial
carcinoma.
• The uterine incision:
– Avoid incisions on the posterior uterine wall, for the
risk of adhesions to the bowel.
– The smallest incision is designed to enable removal of
as many lesions as possible.
– Tunneling in the uterine wall is utilized to minimize
many incisions and peritoneal trauma.
– Try to avoid opening the endometrial cavity.
• To keep the uterus anteverted
– ventrosuspension or plication of the round
ligaments and uterosacral ligaments.
• Dextran solution, Ringer lactate solution or
dexamethazone could be instilled in the
peritoneal cavity to minimize postoperative
adhesions.
Vaginal Procedures
• Vaginal myomectomy:
– Indicated when a fibroid
polyp is not larger than
8 weeks pregnancy
size.
– The polyp is grasped
and twisted until the
pedicle tears.
– If the pedicle is too thick
it is cut with scissors.
– A large polyp could be
cut as piece-meal
fashion (morcellation).
Hysterectomy
• Patient around 40 years, and completed her family.
• The number or site contraindicate myomectomy
• Severe bleeding during myomectomy.
• Major damage of the uterus by myomectomy
which affects its function for pregnancy.
• Recurrent fibroids.
• Suspicious of malignancy
Secondary Changes in Fibroids
• Degenerative
• Vascular
• Inflammatory
• Malignant
Changes
Degenerative Changes
• Hyaline degeneration:
– Commonest secondary change.
– Usually starts around the menopause, and in
the center of the fibroid.
– Macroscopically, fibroid looks homogenous,
waxy, soft, with loss of whorly appearance.
• Fatty changes:
– Likely to start around the age of menopause.
– Lipids reach the fibroid through the blood, so
fatty change starts at the periphery of the
fibroid, resulting in a yellow soft fibroid.
• Calcification:
– Step following fatty change when fatty acids
undergo saponification with Ca salts giving Ca
stearate and palmitate, forming layers of
calcifications.
– Clinically, the fibroid become hard like bone
(Womb stone).
– Radiologically, show a radio-opaque shadow
with typical onion skin appearance.
• Red degeneration (Necrobiosis):
– Usually occurs in the middle trimester of
pregnancy, due to increased vascularity and
venous stasis, the tumor enlarges with
hemorrhage inside the tumor.
– It is called necrobiosis because it shows dead
• Atrophic changes:
– Atrophy occurs due to estrogen withdrawal as
after menopause, puerperium, or anti-estrogen
use.
– All myomas decrease in size after the menopause
except in calcification it remains stationary, or
with malignant change or HRT it increases in
size.
• Myxomatous change:
– Occurs near the menopause, in the center of the
myoma, forming a gelatinous mucoid material
which may undergo pseudo-cystic changes.
• Pseudo-cystic changes:
– A step following hyaline or myxomatous
Vascular Changes
• Torsion (Axial rotation):
–Occurs in moderate-sized, pedunculated, subserous fibroid with no adhesions.
–The precipitating factor is sudden twisting movement as trauma, intestinal
movement, or fetal kick, leading to axial rotation which is prevented from re-twisting
by the lashing effect of the pulsating pedicle.
–The clinical effects depend on the onset of torsion:
• Sudden torsion leads to acute abdomen and necrosis of the tumor.
• Gradual torsion leads to gradual decrease of the blood supply from the pedicle which ends
in the development of parasitic tumor.
• Telangeactasis:
–Likely to occur with pregnancy, malignant change, and cervical fibroid due
to increased vascularity.
–There are numerous dilated blood vessels on the surface of the fibroid
which may
rupture leading to acute abdomen and internal hemorrhage.
• Lymphangeactasis:
–Likely to occur around the age of menopause as the fibroid is full of
lymphatics.
–Dilated lymphatic vessels on the surface may rupture leading to lymphatic
exudates
and strong adhesions.
• Congestion and edema: A result of impaction, incarceration, torsion,
infection,
Inflammatory
changes
• Ways of infection:
– Trauma of submucous fibroid e.g. D & C or
labor.
– Near by inflammation e.g. appendicitis.
– Blood-borne (very rare).
• Result of infection:
– The fibroid becomes congested, tender, and
even abscess formation; it becomes soft and
heals by adhesions to the surrounding
Malignant
changes
• Rare (0.5%) into leiomyosarcoma (round,
spindle, mixed or giant cell histopathology
types).
• Symptoms suggestive:
– The fibroid becomes more painful.
– Post-menopausal bleeding or growth of the tumor.
• Signs suggestive:
– The fibroid become softer, tender, or fixed.
– Rapid growth of the tumor.
Complications of
• Degenerative changes. fibroid
• Vascular changes.
• Inflammatory changes.
• Malignant changes.
• Pregnancy complications e.g. abortion, and preterm
labor.
• Pressure complications on the urethra, bladder,
ureters, rectum, and pelvic veins.
• Rarely, chronic inversion of the uterus.
• Polycythemia and hypertension due to the release
of erythropoietic agent.
• Infertility.
• Secondary parasitic attachment of fibromyomas to
other
abdominal structures gaining another blood supply.
Diagnosis
• After one year of frequent, unprotected sexual
intercourse there is no conception or maintenance of
pregnancy
• 15 – 30% couples in US
Etiology
• Endometriosis
– Interference with tubal patency
– Endometrial fragility
– Adhesions that displace the
ovaries
• Treatment
– Laparoscopy
– Cautery
– Hormonal Rx
Etiology
• Tubal Blockage
– Scarring (PID)
– Fibroids
• Uterine Problems
– Tumors
– Congenital
Anomalies
Etiology
• Anovulation
– Genetic – Turners Syndrome, Hypogonadism
– Problems with the Hypothalamus
• Pituitary-ovarian hormonal feedback
mechanisms
– Hypothyroidism
– Stress
– Decreased body weight
Etiology
• Anovulation
• Treatment
– Menotropins – Pergonal, Repronex (medications made up of
gonadotropins extracted from the urine of postmenopausal
women)
– GnRH Agonist – Lupron, Synarel (synthetic versions of GnRH’s)
Etiology
• Cervical Mucus
Problems
– Vaginal Infections
– Hormone Deficiencies
• Treatment
– HRT
– Cryosurgery
– Guaifenesin
Etiology – Male Factors
• Varicocele – varicose of swollen vein in the
testicle
• Cryptorchidism – undescended testicle at birth
• Restrictive undergarments
• Occupational exposure to heat
• Working in a seated position
Etiology – Male Factors
• Immunological Factors
– Autoimmune reaction
– Production of antibodies that destroy
sperm
• Obstruction in Sperm Transport
– Mumps
– Epididymitis
– STD’s
Assessment – Male History
• General Health
• Nutrition
• Alcohol, drug or tobacco use
• Congenital health problems - hypospadias or
cryptorchidism
• Illnesses such as mumps orchitis, UTI’s, or STD’s
Assessment – Male History
• Operations – surgical repair of a hernia
• Current illnesses – endocrine
• Past and current occupation & work habits (Does job
involve sitting at a desk all day or x-ray exposure)
Assessment – Female History
• Current or past reproductive tract problems
• Endocrine problems
• Abdominal or pelvic surgeries
• Use of vaginal douches or medications (interfere with
pH)
• Occupational exposure to x-ray or toxic substances
Assessment – Female History
• Menstrual History
– Age of menarche
– Length, regularity, & frequency of menstrual
periods
– Amount of flow
– Dysmenorhea / PMS
– Contraceptive use
– Hx. Previous pregnancies or abortions
Diagnostic Studies –
Female
• Basal Body Temperature (BBT)
– Oral temp taken each day prior to arising
– Results are graphed
– Sudden dip occurs the day prior to ovulation & is followed by a
rise of
0.5 –1.0 degrees F, which indicates ovulation
Diagnostic Studies –
Female
• Serum Hormone Testing
– Venous blood is drawn to assess levels of FSH and
LH
– These are indicators of ovarian function
Diagnostic Studies –
Female
• Postcoital Exam
– Couple has sexual intercourse 8 – 12 hours prior to exam, 1-2
days before expected ovulation
– A 10 cc syringe with catheter attached is used to collect a
specimen of secretions from the vagina
– Secretions are examined for: S/S infection, # of active & non-
motile sperm, sperm-mucus interactions, & consistency of cervical
mucus
Diagnostic Studies –
Female
• Endometrial Biopsy
– Paracervical Block to decrease cramping / pain
– Pinch of endometrium obtained to check for a luteal phase
defect (lack of progesterone)
• Pre-procedure Care
– Instruct the client to undress below the waist
– Assist on exam table
Diagnostic Studies –
Female
• Endometrial biopsy

• Post-procedural Care
– Provide sanitary napkins
– Assess for vaso-vagal response – fainting caused by
hypotension
Diagnostic Studies –
Female
• Hysterosalpingogram (HSG)
– Detects uterine anomalies (septate, unicornate, bicornate)
– Detects Tubal anomalies or blockage
– Iodine-based radio-opaque dye is instilled through a catheter into
the uterus and tubes to outline these structures and x-rays are
taken to document findings
Diagnostic Studies –
Female
• Laparoscopy
– General or epidual anesthesia
– Abdomen is insufflated with carbon dioxide
– One or more trochars are inserted into the peritoneum near
the umbilicus & symphysis pubis
– Laparoscope visualizes structures in the pelvis
– Can perform certain surgical procedures
Diagnostic Studies –
Male
• Semen analysis
– Ejaculates into a specimen
container
– Ejaculate examined for:
• Number
• Morphology
• Motility
Normal Semen Analysis Results
• Volume >2.0 mL
• pH 7.0 – 8.0
• Total sperm count >20 million per
mL
• Motility 50% or greater
• Normal forms 50% or greater
Diagnostic Studies –
Male & Female Partner
Anti-sperm antibody evaluation of cervical mucus and
ejaculate are tested for agglutination

Indication that secretory immunological reactions are


occurring between cervical mucus and sperm
Psychological Factors
• Shame
• Guilt
• Stages of grief

• Facilitate
communication
• Listen
• Support Groups
Priority Nursing Diagnosis
• Compromised family
coping
• Knowledge deficit
• Anxiety
• Situational low self-esteem
Implementation and Collaborative Care
• Educational Needs
– Perform various procedures (semen collection)
– Meaning of the results of tests and assessments
– Self-monitoring during medication administration
– How assisted reproductive technologies (ART) are
performed
Implementation and Collaborative Care
• Hormonal Therapy
– How to give SQ and/or IM
injections
Implementation and Collaborative Care
• Medications
– Clomiphene citrate (Clomid, Serophene) – used to increase FSH
and LH secretion, thereby stimulating ovulation
– One IM dose of HCG may be administered to stimulate release of
the ova from the follicles
Implementation and Collaborative Care
• Sperm Washing for Intrauterine Insemination (IUI)
– Ejaculate is centrifuged to concentrate sperm, which are then
rinsed with saline to remove the seminal fluid
– Sperm are again centrifuged, and then used for either IVF
or Intrauterine artificial insemination
Implementation and Collaborative Care
• Intrauterine Insemination (a form of artificial
insemination)
– Sperm are collected within 3 hours of colitus and are inserted
via a catheter into the uterus
– Donor sperm may be used
– Identify of the sperm donor is kept confidential
Implementation and Collaborative Care
• In Vitro Fertilization (IVF)
– Multiple ova are harvested via a large-bore needle and
syringe transvaginally under ultrasound guidance
– Ova are then mixed with sperm
– Up to 4 of the resultant embryos are returned to the uterus 2-3
days later
IVF Side Effects
• Cysts on the ovaries
• Multiple births
• Ovarian
Hyperstimulation
IVF –
Pre-procedure Care
• Administration of synthetic FSH injections SQ in the
abdomen, thigh or upper arm to stimulate the ovary to
produce multiple ova for 5 – 6 days prior to the procedure
• Giving sedation for the oval retrieval procedure
IVF –
Postprocedure Care
• Observation 2 hrs after egg retrieval
• Instructing the woman to limit activity for 24 hrs.
• After embryo placement progesterone supplementation
is commonly prescribed
Alternatives to Childbirth
• Adoption
• Surrogate
mothers
• Childless living
Ca Ovarium
Ca ovarium
• Risk
factor: Risk Factors for Developing Ovarian Cancer
Nulliparity
Early menarche
Late menopause
White race
Increasing age
Residence in North America and northern Europe
Family history
Diagnosis
Signs and Symptoms
• Ovarian cancer typically is portrayed as a "silent killer" without appreciable signs or
symptoms until advanced disease is obvious clinically. This is a misconception. Actually,
patients are often symptomatic for several months before the diagnosis, even with
early- stage disease (Goff, 2000).
• Increased abdominal size, bloating, urinary urgency, and pelvic pain are reported.
Additionally, fatigue, indigestion, inability to eat normally, constipation, and back pain
may be noted (Goff, 2004).
• Abnormal vaginal bleeding occurs rarely. Occasionally, patients may present with nausea,
vomiting, and a partial bowel obstruction if carcinomatosis is particularly widespread.
Unfortunately, many women and clinicians are quick to attribute such symptoms to
menopause, aging, dietary changes, stress, depression, or functional bowel problems. As a
result, weeks or months often pass before medical advice is sought or diagnostic studies
are performed.
Diagnosis
Physical Examination
• A pelvic or pelvic-abdominal mass is palpable in most patients.
• In general, malignant tumors tend to be solid, nodular, and fixed, but there
are no pathognomonic findings that distinguish these growths from benign
tumors.
• Paradoxically, a huge mass filling the pelvis and abdomen more often
represents a benign tumor or low-grade malignancy.
• Ascites -- ascites without a pelvic mass suggests the possibility of cirrhosis
or other primary malignancies such as gastric or pancreatic cancers.
• Auscultation of the chest -- malignant pleural effusions may not be
overtly symptomatic.
• Palpation of the peripheral nodes in addition to a general physical
assessment.
Laboratory Testing
• A routine CBC and metabolic panel often demonstrate a few characteristic features. For
example, 20-25% will present with thrombocytosis (AT > 400 x 109/L). Hyponatremia,
typically ranging between 125 and 130 mEq/L, is another common finding. In these
patients, tumor secretion of a vasopressin-like substance can cause a clinical picture
suggestive of a syndrome of inappropriate antidiuretic hormone (SIADH).
• The serum CA125 test is integral to management of epithelial ovarian cancer. CA125 is a
glycoprotein that may be produced by both benign and malignant ovarian tumors.
• False positive may be associated with a variety of common benign indications, such as
pelvic
inflammatory disease, endometriosis, leiomyomas, pregnancy, and even menstruation.
• With mucinous tumors, the serum tumor markers cancer antigen 19-9 (CA-19-9) and
carcinoembryonic antigen (CEA) may be better indicators of disease than CA125.
Imaging
• Sonography -- To differentiate benign tumors and early-stage ovarian
cancers, transvaginal sonography is typically the most useful imaging
test
• Radiography -- chest radiograph to detect pulmonary effusions or
infrequently, pulmonary metastases. Rarely, a barium enema is helpful
clinically in excluding diverticular disease or colon cancer or in
identifying involvement of the rectosigmoid by ovarian cancer.
• CT Scan -- treatment planning of women with advanced ovarian cancer
• Paracentesis -- A woman with a pelvic mass and ascites can be assumed
to have ovarian cancer until proven otherwise surgically. Thus few
patients require a diagnostic paracentesis to guide treatment.
Staging
Treatment
• Stage I, surgery
• Stage II–IV, usually demonstrated by noninvasive
implants
or nodal metastases, the utility of adjuvant chemotherapy
is speculative
Prevention
• Physical Examination -- annual pelvic examination.
• Chemoprevention -- Oral contraceptive use is associated with a
50- percent decreased risk of developing ovarian cancer.
However, there is a short-term increased risk of developing
breast cancer.
• Prophylactic Surgery -- The only proven way to prevent ovarian
cancer is surgical oophorectomy. As another possible site of
disease among high-risk patients, the fallopian tubes also should
be removed. In BRCA1 or BRCA2 mutation carriers, prophylactic
bilateral salpingo-oophorectomy (BSO) may be performed on
either completion of childbearing or at age 35.
Reference
• Schorge JO, et.al. 2008. Williams Gynecology. The McGraw-
Hill Companies.
Infertilitas
• Masalah yang dihadapi oleh pasangan suami istri yang telah
menikah selama minimal 1 tahun, melakukan hubungan
senggama teratur, tanpa menggunakan kontrasepsi, tetapi
belum berhasil memperoleh kehamilan.

• Infertilitas ini dibagi menjadi 2 yaitu primer dan sekunder


Infertilitas
• Primer : Bila pasangan belum pernah hamil melakukan hubungan seksual secara teratur, tanpa
kontrasepsi dalam periode satu tahun belum ada tanda-tanda kehamilan
• Sekunder : Bila pasangan sudah pernah hamil, dan hubungan seksual teratur tanpa kontrasepsi
tapi belum ada tanda kehamilan

• Infertilitas tidak sama dengan kemandulan (mutlak)


• Infertilitas dikategorikan ketidakmampuan pasangan menghasilkan keturunan,tapi bukan
ketidakmampuan mutlak untuk memiliki keturunan (waktunya ada yg sampai 10 tahun menikah
baru ada tanda kehamilan)
• Kemandulan : sterilitas/ suatu kondisi wanita yang telah diangkat rahimnya (histerektomi) atau
pada laki-laki yang telah dikebiri
Etiologi Infertilitas
• Penyebab utama
– Defek atau disfungsi spermas (25-30%)
– Kegagalan ovulasi (10-20%)
– Kerusakan tuba karena infeksi (10-30%)
– Infertilitas idiopatik (15-25%)
• Penyebab lainnya
– Endometriosis (10-15%)
– Kegagalan atau kurangnya frekuensi koitus (3-4%)
– Disfungsi atau defek mukus serviks (3-5%)
– Abnormalitas uterus
– Tuberkulosis genital
– Penyakit yang menyebabkan kelumpuhan
Etiologi
• Faktor tuba dan pelvik (sumbatan atau kerusakan tuba akibat
perlekatan atau akibat endometriosis)
• Faktor lelaki (abnormalitas jumlah, motilitas, morfologi
sperma)
• Disfungsi ovulasi (ovulasi jarang atau tidak ada ovulasi)
• Idiopatik
• Lain-lain (fibroid, polip endometrium, kelainan bentuk uterus)

(sumber: Kandungan/ Editor Mochammad Anwar tahun 2011).


Infeksi
• Kuman pnybab : GO, TBC, klamiadia mikoplasma hominis, klmpok entrero bakteria,
HSV2, HPV, EBV, CMV, HB, Hiv, E.coli, trikomonas, virus mumps, lues, candida
• Analisa semen:
- Lekositospermia
- Mobilitas sperma menurun
- Konsentrasi spermatozoa menurun
- Persentase morfologi abnormal spermatozoa meningkat
- Aglutinasi jenis kepala kepala
• Terapi
Antibiotik
Jenisnya tergnatung kuman penyebab
Infertilitas pada reproduksi wanita

• Gangguan pada ovulasi –> tidak ada ovum yang matang


• Gangguan pada tuba uterine –> sumbatan atau perlekatan
pada tuba uterine.
• Catatan : ovum matang hanya bertahan 24 jam. Jika tidak
dibuahi dalam 24 jam maka tidak terjadi embrio.
• gangguan hormon (FSH, LH, Estrogen dan progesteron)
• gangguan uterus / rahim (infeksi / tumor)
• antibodi terhadap sperma
Faktor Predisposisi
• Non-Organik
– Usia
– Frekuensi Senggama
– Alkohol
– Merokok
– Obesitas
• Organik
– Vagina (dispareunia, vaginismus, vaginitis)
– Uterus (servisitis, trauma pada serviks, kelainan kavum uteri, endometriosis, polip endometrium,
mioma uteri, adenomiosis)
– Tuba (striktur tuba)
– Ovarium (gangguan fungsi ovulasi)
– Peritoneum

(sumber: Kandungan/ Editor Mochammad Anwar tahun 2011).


Non-Organik
• Usia
Terutama usia istri, sangat menentukan besarnya kesempatan
pasangan suami-istri untuk mendapatkan keturunan.
Akibat masalah ekonomi, meletakan kehamilan sebagai prioritas
kedua setelah upaya mereka meraih jenjang jabatan yang baik
merupakan alasan perempuan untuk menunda kehamilan.
• Frekuensi Senggama
Angka kejadian kehamilan mencapai puncaknya ketika pasangan
suami-istri melakukan hubungan dengan frekuensi 2-3 kali
seminggu.
Upaya penyesuaian saat melakukan hubungan dengan terjadinya
ovulasi, akan meningkatkan kejadian stress bagi pasangan suami-
istri tsb.
• Pola Hidup
- Alkohol
Bagi laki-laki, alkohol dapat menurunkan kualitas sperma

- Merokok
Rokok dpt menurunkan fertilitas perempuan perokok aktif, maupun pasif. Penurunan
fertilitas juga dialami oleh lelaki yang memiliki kebiasaan merokok

- Berat Badan
Perempuan obesitas (IMT >29) terbukti mengalami keterlambatan hamil. Usaha terbaik
untuk menurunkan BB adalah dengan olahraga serta mengurangi asupan kalori
Organik

A. Masalah Vagina
Terjadinya proses reproduksi manusia sangat terkait dengan
kondisi vagina yang sehat dan berfungsi normal. Masalah pada
vagina memiliki kaitan erat dengan peningkatan kejadian
infertilitas.
• Dispareunia
Merupakan masalah kesehatan yang ditandai dengan rasa tidak
nyaman atau rasa nyeri saat melakukan sanggama

Pada perempuan dpt disebabkan oleh bbrp faktor antara lain:


- Faktor infeksi: kandida, chlamydia trakomatis, trikomonas vaginalis
- Faktor organik: vaginismus, nodul endometriosis atau keganasan
vagina.
Pada laki-laki dpt disebabkan oleh:
- Faktor infeksi: uretritis, prostitis atau sistitis. Disebabkan oleh
kuman infeksi, N.gonore.
- Faktor organik: prepusium terlampau sempit, luka di penis
akibat infeksi sebelumnya dsb.
• Vaginismus
Merupakan masalah pada perempuan yang ditandai dengan
adanya rasa nyeri saat penis melakukan penetrasi ke dalam
vagina.
Disebabkan oleh diameter liang vagina yang terlalu sempit,
akibat kontraksi otot pubokoksigeus yang terlalu sempit.
B. Masalah uterus

• Faktor serviks
- Servisitis: menyebabkan kesulitan sprema untuk masuk ke dalam
kavum uteri

- Trauma pada serviks: tindakan operatif tertentu pada serviks


sehingga menyebabkan cacat pada serviks, dpt menjadi penyebab
infertilitas
C. Masalah Ovarium
Masalah utama yang terkait dengan fertilitas adalah terkait
dengan fungsi ovulasi. Sindrom ovarium polikistik merupakan
masalah gangguan ovulasi utama.
• Saat ini untuk menegakan diagnosis sindrom ovarium polikistik
bila dijumpai 3 gejala berikut:
- Siklus haid oligoovulasi atau anovulasi
- Gambaran ovarium polikistik pada pemeriksaan USG
- Gambaran hiperandrogenisme baik klinis maupun biokimiawi
Gangguan Serviks
Hal yang berkontribusi pada infertilitas:
• Sumbatan kanalis servikalis
• Lendir serviks yang abnormal
• Malposisi dari serviks
Pemeriksaan untuk menilai serviks:
• Uji pascasanggama
– Menilai banyaknya spermatozoa pada lendir serviks pasca sanggama
dalam 1 LPB
• Uji gelas objek
– Menilai kemampuan spermatozoa untuk masuk ke dalam lendir
serviks
• Uji kontak air mani
– Membandingkan motilitas sperma pada lendir serviks dan air mani
Gangguan Uterus
Hal yang berkontribusi pada infertilitas:
– Dikaitkan dengan kemampuan uterus untuk membantu transportasi
spermatozoa
– Masalah yang ditemukan:
• Gangguan kontraksi uterus
• Distorsi kavum uteri
• Peradangan endometrium
– Pemeriksaan:
• Biopsi endometrium
• Histerosalpingografi
• Histeroskopi
Gangguan Tuba
• Hal yang berkontribusi pada infertilitas:
– Penyebab tersering infertilitas
– Pemeriksaan berupa pertubasi
• Meniupkan gas CO2 melalui kateter atau kanula yang dipasang pada kanalis
servikalis untuk melihat patensi tuba
• Kontraindikasi: kehamilan, baru dilakukan kuretase, perdarahan uterus, dan
peradangan alat kelamin
Gangguan Ovarium
• Pemeriksaan gangguan ovarium
– Untuk melihat ada tidaknya ovulasi
– Pemeriksaan mencakup:
• Penilaian lendir serviks
• Catatan suhu basal badan
• Sitologi vagina hormonal
• Pemeriksaan hormonal
• Biopsi endometrium
Gangguan Peritoneum
Laparoskopi diagnostik-> tahapan akhir dari pengelolaan
infertilitas
– Indikasi uji diagnostik ini:
• Selama satu tahun pengobatan, belum terjadi kehamilan
• Siklus haid yang tidak teratur atau suhu basal yang monofasik
• Apabila istri pasangan infertil berumur 28 tahun atau lebih
mengalami infertilitas selama 3 tahun lebih
• Pernah dilakukan histerosalpingografi dengan media kontras larut
minyak
• Terdapat riwayat appendisitis
• Pertubasi berkali-kali menunjukkan hasil abnormal
• Dicurigai terjadi endometriosis
• Apabila akan dilakukan inseminasi buatan
Pemeriksaan Penunjang pada Infertilitas
• Pada pria : analisis sperma (setelah abstinensi 2-3 hari)
– Karakteristik air mani
• Koagulasi dan likuefaksi : saat ejakulasi cair, setelah 5-20 menit
mengalami likuefaksi  pekat.
• Viskositas (pipet Ellison).
• Warna dan bau : putih kelabu, setelah likuefaksi  jernih atau keruh.
Bau seperti bau bunga akasia.
• Volume : 1-5cc.
• pH : 7,3-7,7.
• Uji fruktosa (+).
– Mikroskopik
• Konsentrasi spermatozoa ≥40jt dengan densitas ≥20jt/cc.
• Motilitas spertmatozoa setelah 2-3 jam, 60% masih bergerak.
• Uji ketidakcocokan imunologik.
TERMINOLOGI DAN DEFINISI ANALISIS SPERMA
BERDASARKAN KUALITAS SPERMA
Terminologi Definisi
Normozoospermia Ejakulasi normal sesuai nilai rujukan
WHO (normal : 20 juta/ml atau >)
Oligozoospermia Konsentrasi sperma < nilai rujukan WHO
Astenospermia Konsentrasi sperma dengan motilitas <
nilai rujukan WHO
Azoospermia Tidak didapatkan sel sperma dalam
ejakulat
Aspermia Tidak terdapat ejakulat
Kristospermia Jumlah sperma sangat sedikit.
Didapatkan setelah sentrifugasi

Medical Mini Notes. Gynecologic. Medical Mini Notes


Production; 2014.
Medikamentosa

1. Clomiphene citrate (anti estrogen)


- Cara kerja : ikat reseptor estrogen hipoT & hipo F
 stop umpan balik (-)  ovulasi dapat terjadi
- Derivat Non steroid triphenylethlene
- Indikasi : tidak folikel > 20mm dan endometrium <
5mm
- Termasuk Kategori X (FDA) PASTIKAN TIDAK HAMIL
- Dose : 50mg/day oral – 5 hari (50-250mg/hr)
Medikamentosa

2. Gonadotropin
- Untuk pasien dgn “clomiphene resistent”
- Step up (50-74 iu/day  increase) dan step down
(hati” ovarian hiperstimulation syd)
- ES : Multifetal gestation dan ovarian
hiperstimulation syd
Medikamentosa

3. Aromatase inhibitor (letrozole – femara)


- Keuntungan : es < gonadotropin , less expensive
- Fungsi : turunin sintesis estrogen dan menaikkan
tertosteron  meningkatkan spematogenesis

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