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Retrograd darah haid

The transplantation theory, originally proposed by Sampson in the mid-1920s, is based on the
assumption that endometriosis is caused by the seeding or implantation of endometrial cells by
transtubal regurgitation during menstruation (30) . Substantial clinical and experimental data support
this hypothesis (5,31). Retrograde menstruation occurs in 70% to 90% of women, and it may be more
common in women with endometriosis than in those without the disease. The presence of endometrial
cells in the peritoneal fluid, indicating retrograde menstruation, is reported in 59% to 79% of women
during menses or in the early follicular phase, and these cells can be cultured in vitro (33,34). The presence
of endometrial cells in the dialysate of women undergoing peritoneal dialysis during menses supports the
theory of retrograde menstruation (35). Endometriosis is most often found in dependent portions of the
pelvis—the ovaries, the anterior and posterior cul-de-sac, the uterosacral ligaments, the posterior uterus,
and the posterior broad ligaments (36). The menstrual reflux theory combined with the clockwise
peritoneal fluid current explains why endometriosis is predominantly located on the left side of the pelvis
(refluxed endometrial cells implant more easily in the rectosigmoidal area) and why diaphragmatic
endometriosis is found more frequently on the right side (refluxed endometrial cells implant there by the
falciform ligament)

Coelemik metaplasia

The transformation (metaplasia) of coelomic epithelium into endometrial tissue is a proposed

mechanism for the origin of endometriosis. One study evaluating structural and cell surface antigen
expression in the rete ovarii and epoophoron reported little commonality between endometriosis and
ovarian surface epithelium, suggesting that serosal metaplasia is unlikely in the ovary (57). The results of
another study involving the genetic induction of endometriosis in mice suggest that ovarian endometriotic
lesions may arise directly from the ovarian surface epithelium through a metaplastic differentiation
process induced by activation of an oncogenic K-ras allele

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Stem cell

Endometrial stem cells are identified, are bone marrow derived, can differentiate into neurogenic or
pancreatic-β cells, may contribute to the development of endometriosis in a murine model, and their
potential role in the pathogenesis of endometriosis needs to be investigated

Pembuluh darah dan limfe

Ovarian endometriosis may be caused by either retrograde menstruation or by lymphatic flow from the
uterus to the ovary; metaplasia and bleeding from a corpus luteum may be a critical event in the
development of some endometriomas. Extrapelvic endometriosis, although rare (1% to 2%), may result
from vascular or lymphatic dissemination of endometrial cells to many gynecologic (vulva, vagina, cervix)
and nongynecologic sites. The latter include bowel (appendix, rectum, sigmoid colon, small intestine,
hernia sacs), lungs and pleural cavity, skin (episiotomy or other surgical scars, inguinal region, extremities,
umbilicus), lymph glands, nerves, and brain

Teori genetik dan inflamasi

The induction of humanlike endometriosis by genetic activation of an oncogenic K-ras allele lends further
support to the genetic basis of this disorder. Although retrograde menstruation appears to be a common
event in women, not all women who have retrograde menstruation develop endometriosis. The immune
system may be altered in women with endometriosis, and it is hypothesized that the disease may develop
as a result of reduced immunologic clearance of viable endometrial cells from the pelvic cavity (80,81).
Endometriosis can be caused by decreased clearance of peritoneal fluid endometrial cells resulting from
reduced natural killer (NK) cell activity or decreased macrophage activity. Endometriosis is associated with
a state of subclinical peritoneal inflammation, marked by an increased peritoneal fluid volume, increased
peritoneal fluid white blood cell concentration (especially macrophages with increased activation status),
and increased inflammatory cytokines, growth factors, and angiogenesis-promoting substances.

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Pain

Dysmenorrhea often starts before the onset of menstrual bleeding and continues throughout the
menstrual period. In adolescents, the pain may be present after menarche without an interval of pain-
free menses. The distribution of pain is variable but most often is bilateral. Local symptoms can arise from
rectal, ureteral, and bladder involvement, and lower back pain can occur. Some women with extensive
disease have no pain, whereas others with only minimal to mild disease may experience severe pelvic
pain. All endometriosis lesion types are associated with pelvic pain, including minimal to mild
endometriosis. Possible mechanisms causing pain in patients with endometriosis include local peritoneal
inflammation, deep infiltration with tissue damage, adhesion formation, fibrotic thickening, and collection
of shed menstrual blood in endometriotic implants, resulting in painful traction with the physiologic
movement of tissues (177,178). The character of pelvic pain is related to the anatomic location of deeply
infiltrating endometriotic lesions (171). Severe pelvic pain and dyspareunia may be associated with deep
infiltrating subperitoneal endometriosis (6,177,179). In rectovaginal endometriotic nodules, a close
histologic relationship was observed between nerves and endometriotic foci and between nerves and the
fibrotic component of the nodule (180). Increasing evidence suggests a close relationship between the
density of innervation of endometriotic lesions and pain symptoms (

Infertility

When endometriosis is moderate or severe, involving the ovaries and causing adhesions that block tubo-
ovarian motility and ovum pickup, it is associated with subfertility

Endometrioma

I don’t know HAHAHAHAHAHAH

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PANDUAN PRAKTIK KLINIS MEDIS

SMF : OBSTETRI DAN GINEKOLOGI
RSUP DR. HASAN SADIKIN

ENDOMETRIOSIS
Batasan Ditemukannya jaringan menyerupai kelenjar dan stroma endometrium di luar uterus.
Endometriosis merupakan kelainan jinak, bersifat kronis, dan tergantung estrogen.
Faktor risiko Pertumbuhan dan keberlangsungan implan endometriosis dibawah pengaruh steroid
ovarium.

Gejala Klinis Dismenore

Nyeri Pelvik
Dispareunia
Gangguan usus (konstipasi, diare)
Nyeri usus
Infertilitas
Kista Ovarium
Disuria
Diagnosis 1. Anamnesis
2. Pemeriksaan fisik:
 Serviks tertarik ke satu sisi akibat dorongan/tarikan implan di cavum Douglas
atau ligamentum uterosakral
 Nodul nyeri di daerah cul-de-sac, ligamentum uterosakral, atau septum
rektovaginal
 Penebalan dan indurasi ligamentum uterosakral
 Nyeri goyang uterus
 Massa yang nyeri di adneksa
 uterus terfiksasi ke posterior .
 Laboratorium: tidak ada yang sensitif
 USG: kista endometrioma
 Laparoskopi diagnostik: visualisasi implan
Diagnosis diferensial Kehamilan ektopik, PID, interstitial cystitis, adenomyosis, neoplasma ovarium, adhesi pelvik,
irritable bowel syndrome, kanker kolon, diverticular disease, dan splenosis
Klasifikasi Berdasarkan American Society for Reproductive Medicine (ASRM) 1979 dan revisi 1996:
Stage I : minimal, implan terisolir,tanpa adhesi..
Stage II : mild endometriosis, implan superfisial < 5 cm di
peritoneum dan ovarium. Tanpa adhesi..
Stage III : moderate, implan multipel, baik superfisial dan invasif.
disertai adhesi peritubal dan periovarian.
Stage IV : berat, implan superfisial dan dalam, kista endometrioma
yang besar. Adhesi serabut padat.
Pengobatan Pilihan terapi:
a) Managemen ekspektasi
b) Analgesia: memblok prostaglandin (asam mefenamat)
c) Hormonal:
- Medroksi progesteron asetat 5-10 mg/hari atau norethindrone asetat 5
mg/hari selama 6 bulan.

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-Depot medroxyprogesterone acetate (DMPA) tiap 3 bulan.

-LNG-IUD tiap 5 tahun.
-Etonogestrel subdermal implant selama 1 tahun.
-Dienogest 2 mg/hari
-Kontrasepsi kombinasi estrogen-progestin
-Gonadotropin-releasing hormone (GnRH) agonists: nyeri moderat atau
berat selama 3-6 bulan.
- Danazol 400 - 800 mg /hari selama 6 bulan
- Aromatase inhibitor: anastrozole (1 mg) atau letrozole (2,5 mg/hari)
d) Operasi:
bila terapi medisinal gagal atau mempunyai kontraindikasi terapi medisinal,
memerlukan diagnosis yang lebih pasti selain menyingkirkan keganasan
dan memperbaiki fertilitas pada wanita yang tidak dapat menjalani induksi
ovulasi dan inseminasi/program IVF.
- Reseksi dan ablasi implan endometriosis
- kistektomi atau
- histerektomi dan bilaterai salpingo-oforektomi
e) Kombinasi terapi medikal pre/post operasi:
Pemberian hormonal pasca-operasi: pil kontrasepsi
kombinasi, progestin, LNG-IUD atau GnRHagonist.

PANDUAN PRAKTIK KLINIS

MEDIS

PANDUAN PRAKTIK KLINIS MEDIS

SMF : OBSTETRI DAN GINEKOLOGI
RSUP DR. HASAN SADIKIN

ADENOMIOSIS
Batasan Ditemukannya kelenjar dan stroma endometrium di lapisan otot rahim (uterine
adenomyomatosis).
Pathogenesis berasal dari invaginasi endometrium ke endomyometrial atau de novo sisa mullerian

Gejala Klinis - Haid yang banyak dan nyeri

- Nyeri Pelvik kronik
- Dismenore
- Infertilitas
Diagnosis - USG transvaginal
- magnetic resonance imaging (MRI).
- Pemeriksaan histologi dari jaringan histerektomi.
Diagnosis diferensial Kehamilan, leiomioma, endometriosis, dan polip endometrium, mioma submukosa,
hiperplasia endometrium, sinekia, adenokarsinoma, atau infeksi (endometritis)
Pengobatan/Penanganan - Histerektomi bila anak cukup. Bila menolak histerektomi lakukan
reseksi adenomyosis dan terapi lain untuk menghilangkan nyeri.
- Terapi dengan progestins (termasuk levonorgestrel-releasing
intrauterine contraception [IUC]), gonadotropin releasing hormone
analogs, atau aromatase inhibitor efektif untuk menorrhagia dan
dysmenorrhea.

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- Terapi nyeri lain menggunakan kontrasepsi kombinasi estrogen-

progestin kontinyu