Transcript Document
ENDOMETRIOSIS
DYSMENORRHEA &
CHRONIC PELVIC PAIN
Endometriosis
(definition)
The presence of endometrial tissue in
extrauterine locations .
Endometriosis - pathogenesis
The exact pathogenesis is unknown
Three theories:
1. Theory of the implantation (Sampson´s
theory) – direct implantation of endometrial
cells, typically by means of retrograde
menstruation.
Endometriosis - pathogenesis
2. Coelomic metaplasia of multipotential cells
in the peritoneal cavity (Meyers theory)
states that, under certain conditions m-p
cells can develop into endometrial tissue
3. Vascular and lymphatic dissemination of
endometrial cells (Halbans theory) – distant
sites of endometriosis can be explained by
this process ( lymph nodes, pleura, kidney)
Endometriosis
division by Semm
Internal endometriosis of genital organs
• Adenomyosis
(endometrial tissue in uterine wall)
• Adenomyoma
(endometrial tissue in uterine myomas)
• Endometriosis in the wall of uterine tube
Endometriosis
division by Semm
External endometriosis of genital organs:
• Ovary:
- endometrioma
(the endometrial tissue deeply in ovary tissue
as a tumor)
- on the surface of ovary.
• Uterosacral ligaments, round ligament
of the uterus.
• Uterine tubes
Endometriosis
division by Semm
External endometriosis of genital organs:
•
•
•
•
•
Anterior et posterior cul-de-sacs
Pelvic peritoneum over uterus
Uterine cervix
Fornix of the vagina, vagina
Perineum
Endometriosis
division by Semm
Extragenital endometriosis
• Sigmoid colon, ampula of the rectum,
cecum, appendix
• Urinary bladder
• Umbilicus
• Postoperative scars
(laparotomia, cesarean section)
Endometriosis
division by Semm
Extragenital endometriosis
•
•
•
•
•
•
•
Omentum
Small intestine
Femoral canal
Arms, legs
Lungs, pleura
Brain
Kidney
Endometriosis
the most common sites
•
•
•
•
Surface of the ovary –60 – 70%
Endomerioma (ovary)– 30-40%
Peritoneum over the uterus – 40-50%
Uterine tube and mesosalpinx – 20 –
30%
• Posterior cul –de –sac - 20- 30%
• Uterosacral ligaments - 20-25%
• Rectosigmoid - 7-10%
Endometriosis
symptoms
•
•
•
•
•
•
Pelvic pain
Dysmenorrhea
Dyspaurenia
Dysuria, hematuria
Dyschesia, rectal bleeding
Abnormal bleeding
(irregular menstrual periods, premenstrual
spotting)
Endometriosis
complications
• Infertility
• Abortions
• Acute abdominal emergency
(rupture or torsion of an
endometrioma)
Infertility
• In the group of infertile women the
endometriosis occurs in 30-50%
• In the group of women with the
endometriosis infertility occurs in 30-70%
The higher stage of endometriosis –
the lower chance of pregnancy.
Infertility
reasons
• Distortion of the elements of the reproductive tract
and damage to the ovary (obstruction of the uterine
tube, adhesions, cysts)
• Functional infertility (the influence of prostaglandin,
IL-5, IL-6, complement: C3,C4 macrophages, LT
helper, LT supresors, NK - anovulation, luteal phase
inadequacy, phagocytosis of sperm, oocytes,
unproper conditions to the implantation
Endometriosis
the risk factors
• Congenital anomalies that promote
retrograde menstruation
• Short period, long lasting menstruation
• Dysmenorrhea
• Infertility
• First and second degree relatives have
had endometriosis
Endometriosis
diagnosis
• Anamnesis
• Physical examination
• Laboratory studies are not useful at
making the diagnosis but helpful in the
differential diagnosis
• Pelvic ultrasound
• Laparoscopy
• Histopathological examination
Endometriosis
diagnosis
• Establishing
a diagnosis
requires
direct visualisation at the time of the
diagnostic
laparoscopy
or
the
laparotomy
• Histopatological confirmation of
endometriosis is „the gold standard”
Laparoscopy / Laparotomy
description of the lesions
• Peritoneum: vascular hemorrhagic areas,
white - opaque plaques, spots described as
„mulberry” or „raspberry”, fibrosis surrounding
these lesions, adhesions
• Ovary : endometriomas – filled with thick,
chockolate-appearing fluid; superficial
implants
• Uterine tubes: tubal occlusion, adhesions,
distortion
• Uterus: superficial implants, retroverted and
fixed
Endometriosis
staging
Classification system by the AFS
•
•
•
•
•
Stage I – minimal
1-5
Stage II – mild
6-15
Stage III – moderate
16-40
Stage IV – severe
>40
Evaluation of areas of endometriosis
(size,localization); adhesions (types,
localization), posterior cul-desac obliteration,
tubal occlusion
Endometriosis
differential diagnosis
• Abdominal pain
( PID, GI dysfunction, adhesions, tumors)
• Dysmenorrhea
• Dyspaurenia
(PID, colpitis, uterine retroversion)
• Abnormal bleeding
(hormonal dissfunction, polyps, cervical
lesions)
Endometriosis
differential diagnosis
• Acute abdominal emergency
(ectopic pregnancy, adnexal torsion,
rupture
of corpus luteum, acute PID –
peritonitis)
• Dysuria, dyschesia, hematuria,
rectal beeding, hemoptysis, tumor
in the scar - rare symptoms
Endometriosis
treatment
The choice of therapy depends on
• Presenting symptoms and their severity
• Location and severity of endometriosis
• Desire for future childbearing
Endometriosis
treatment
3 stages of the treatment by Semm
• I stage: laparoscopy - surgical tratment:
electrocoagulation of endometriosis, removal
of the cysts and adhesions
• II stage: medical therapy 3 – 6 months
• III stage: surgical therapy – removal of
remaining endometriosis, salpingoplasty
Endometriosis
medical therapy
3 groups of medicines:
1. Danazol
2. Progestins
3. Gonadotropin-releasing hormone
agonists
Progestins
endometriosis treatment
• Medroxyprogesterone acetate
Provera tb 20 – 40 mg/d
• Depomedroxyprogesterone acetate
Depo-Provera inj. i.m. 100 mg /
2 weeks – 8 weeks,
than 200 mg/1 month
Progestins
endometriosis treatment
Progestins supress FSH/LH release
and ovarian steroidogenesis
„pseodopregnancy”
Progestins
endometriosis treatment
• Adverse effects:
nervous system - depresion, headache,
vertigo, nervosity;
skin - oily skin, itch, hirsutism;
mastalgia, nausea, weight gain;
thrombosis, alterations of lipoprotein,
glucose and Ca and P metabolism
Danazol
endometriosis treatment
• Danazol-17α-ethinyl testosterone
derivative
tb 600 - 800 mg/d – 1 month, than 400
mg up to 6 months
• Supresses FSH/LH release and
steroidogenesis endometrial atrophy
„pseudomenopause”
Danazol
endometriosis treatment
• Adverse effects: hypoestrogenic and
androgenic properties: acne , oily skin,
hirsutism, spotting, bleeding, hot flushes,
atrophic vaginitis nausea, depresion,
nervosity, headache, vomit, alterations of
lipoprotein, glucose, Ca and P metabolism
GnRh agonists
endometriosis treatment
• Triptorelin –
Decapeptyl depot a 3.75 mg inj i.m. 1x/28d,
Dipherelinum SR a 3.75 mg inj i.m. 1x/28d
• Goserelin –
Zoladex a 3.6 mg inj s.c 1x/28d
Therapy 3 – 6 months
GnRh agonists
endometriosis treatment
• Pituitary desensybilisation
supress FSH/LH release
„a state of pseudomenopase”
GnRh agonists
endometriosis treatment
• Adverse effects:
hypoestrogenic propierties
without
androgenic effects
• The most expensive therapy but
the most effective one
DYSMENORRHEA
PAINFUL MENSTRUATION
• Primary (absence of demonstrable
pelvic disease)
• Secondary (presence of pelvic
pathology – endometriosis, chronic PID,
uterine leiomyomas)
HOW TO DISCOVER THE CAUSE
OF DYSMENORRHEA ?
•
•
•
•
Diagnostic laparoscopy
Empiric drug therapy
USG, RTG, MRT, CT
Laboratory tests
PRIMARY
DYSMENORRHEA
• Begins with the onset of menstruation and
lasts 12 – 72 hours
• Pain in lower abdomen, most intense in the
midline
• Pain described as crampy and intermittent,
sometimes back pain and thigh pain
• Accompanied by nousea, diarrhea, fatigue,
headache
CAUSIVE AGENTS
Released from the endometrium PGE2 and
PGF2 induce smooth muscle contraction in
many tissues.
Contraction of the uterus can exceeds 60 mm
Hg - uterine ischemia – accumulation of
anaerobic metabolites (acidosis) –
stimaulation of type-C pain neurons.
PATHOPHYSIOLOGY
High rates of endometrial prostaglandin
production require the sequential
stimualation by estrogen followed by
progesterone – anovulatory cycles are
mostly painless.
SECONDARY
DYSMENORRHEA
•
•
•
•
•
Is connected with pelvic pathology
Usually begins after age of 20
Often lasts for 5 – 7 days monthly
Has increased in severity
Some women have markedly abnormal
pelvic examination
TREATMENT
• ANTIINFLAMMATORY AGENTS (inhibition of
prostaglandin production and action)
IBUPROFEN (arylopropionic acid derivative)
4 x 400 mg/24 h for 3 – 4 days
NAPROXEN (mefanemic acid or it’s sodium salts)
• ORAL CONRACEPTIVES
(suppress endometrial PG production by inhibiting ovulation)
INHIBITORS OF PG
SYNTHESIS
GRUG CLASS
Fenamates
Phenylopropionic
acid
DRUG
STANDARD DOSE
Mefenamic acid
500 mg than 4 x 250
mg/24 h
Flufenamic acid
3 x 100-200 mg/24 h
Tolfenamic acid
3 x 133 mg/24 h
Ibuprofen
4 x 400 mg/24 h
Naproxen sodium
550 mg than 4 x 275
mg/24 h
Ketoprofen
3 x 50 mg/24 h
CHRONIC PELVIC PAIN
Complain presentig in 10% to 30% of all
gynecologic visits
12% to 19% of all hysterectomies are
performed because of unresolved
chronic pain
Three dimensions defining
chronic pelvic pain
DIURATION - any type of pelvic pain lasting
longer than 6 months
ANATOMIC – defined by physical findings at
laparoscopy
AFFECTIVE/BEHAVIORAL – pain accompanied
by significant altered physical activity
Ethiology
• Pelvic pathology (adhesions, endometriosis,
ovarian cysts)
• Unidentifiable pathology
• Nongynecologic causes (constipations, irritable
bowel syndrome, urethral syndrome, interstitial
cystitis, bladder spasms, musculosceletal
problems, psychiatric comorbidity,
psychopathology).
MULTIDISCIPLINARY TREATMENT IS REQUIRED.