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ENDOMETRIOSISENDOMETRIOSIS
Syeda Komal Siraj
08-195
 Endometriosis is a disease or better a syndromeEndometriosis is a disease or better a syndrome
that starts around the prepubertal age,that starts around the prepubertal age,
flourishing after menarche, with symptomsflourishing after menarche, with symptoms
progressing in intensity through the years.progressing in intensity through the years.
 Predominantly found in women of reproductivePredominantly found in women of reproductive
ageage
 Found in all the ethnic & social groupsFound in all the ethnic & social groups
DEFINITIONDEFINITION
 EndometriosisEndometriosis (from(from endoendo, "inside", and, "inside", and metrametra, ", "wombwomb""
 Presence of endometrial like tissue (glands/stroma)Presence of endometrial like tissue (glands/stroma)
outside the uterus which induces chronic inflammatoryoutside the uterus which induces chronic inflammatory
reaction.reaction.
 Most frequent sites are pelvic viscera & peritoneum outMost frequent sites are pelvic viscera & peritoneum out
of which most common site is ovary (RCOG guidelineof which most common site is ovary (RCOG guideline
no. 24, 2006)no. 24, 2006)
 Adenomyosis is ectopic endometrium inside theAdenomyosis is ectopic endometrium inside the
myometrium of uterus, previously known asmyometrium of uterus, previously known as
endometriosis interna.endometriosis interna.
INCIDENCEINCIDENCE
• Asymptomatic women undergoing tubal sterilizationAsymptomatic women undergoing tubal sterilization
i.e. women with proven fertility - 7%i.e. women with proven fertility - 7%
• Primary infertility (20-30%)Primary infertility (20-30%)
• Dysmenorrhoea (40-60%)Dysmenorrhoea (40-60%)
• Chronic pelvic pain(71-80%)Chronic pelvic pain(71-80%)
ETIOLOGYETIOLOGY
 Exact etiology of endometriosis is unknown.Exact etiology of endometriosis is unknown.
 Understanding of endometriosis is just a beginning.Understanding of endometriosis is just a beginning.
 It is a estrogen dependent disease.It is a estrogen dependent disease.
HYPOTHESISHYPOTHESIS
1.1. Retrograde menstruation/ectopic transplantation/Retrograde menstruation/ectopic transplantation/
Sampson’s theory –Sampson’s theory –
(Lancet, 2004
• Most widely recognized & plausible theory on the genesisMost widely recognized & plausible theory on the genesis
of endometriosis.of endometriosis.
• Based on the assumption that endometriosis is causedBased on the assumption that endometriosis is caused
by the seeding or implantation of endometrial cell byby the seeding or implantation of endometrial cell by
trans tubal regurgitation during menstruation.trans tubal regurgitation during menstruation.
• Supported by – Blood can be found in peritoneal cavitySupported by – Blood can be found in peritoneal cavity
on laparoscopy during menstruation in 75-90%on laparoscopy during menstruation in 75-90%
- most often found in dependent portions- most often found in dependent portions
of the pelvis like ovaries, anterior & posterior cul-de-sac,of the pelvis like ovaries, anterior & posterior cul-de-sac,
the uterosacral ligaments, posterior uterus, posteriorthe uterosacral ligaments, posterior uterus, posterior
broad ligaments.broad ligaments.
 More in women with stenosis of internal osMore in women with stenosis of internal os
 Mullerian abnormalitiesMullerian abnormalities
2.2. Coelomic Metaplasia/ MetaplasticCoelomic Metaplasia/ Metaplastic
Transformation/ Meyer’s theoryTransformation/ Meyer’s theory --
 Both peritoneal and endometrial tissues share aBoth peritoneal and endometrial tissues share a
common embryologic precursor the coelomic cell.common embryologic precursor the coelomic cell.
 Metaplastic transformation of coelomic epitheliumMetaplastic transformation of coelomic epithelium
into endometrial tissue can occur.into endometrial tissue can occur.
 Premenarchal girl who have never menstruatedPremenarchal girl who have never menstruated
 Unusual sites( Extremities, brain, pleura)Unusual sites( Extremities, brain, pleura)
33. Lymphatic or Hematogenous Spread Distant to. Lymphatic or Hematogenous Spread Distant to
pelvis/ Hallban’s theory –pelvis/ Hallban’s theory –
 Explain the observation of endometriosis in unusualExplain the observation of endometriosis in unusual
sites such as brain & pleurasites such as brain & pleura
 Extra pelvic endometriosis - vascular or lymphaticExtra pelvic endometriosis - vascular or lymphatic
dissemination of endometrial cellsdissemination of endometrial cells
 Ovarian endometriotic lesion may arise directly fromOvarian endometriotic lesion may arise directly from
ovarian surface epithelium through a metaplasticovarian surface epithelium through a metaplastic
differentiation process induced by activation of andifferentiation process induced by activation of an
oncogenic K-ras allele.oncogenic K-ras allele.
 Ovarian endometriosis - retrograde menstruation orOvarian endometriosis - retrograde menstruation or
lymphatic flow from the uterus.lymphatic flow from the uterus.
4.4. Direct Transplantation from Tissue Trauma orDirect Transplantation from Tissue Trauma or
SurgerySurgery
 Explain the finding of localized endometriosisExplain the finding of localized endometriosis
cesarean-section scar or episiotomy sites.cesarean-section scar or episiotomy sites.
• Biologically distinct tissue may directly attach to aBiologically distinct tissue may directly attach to a
site accompanied by initiation of localized oncogenic-site accompanied by initiation of localized oncogenic-
like cascades leading to implant survival.like cascades leading to implant survival.
• Decreased immunosurveillance which wouldDecreased immunosurveillance which would
normally clear the ectopic tissue--may also be therenormally clear the ectopic tissue--may also be there
5.5. Induction theory –Induction theory –
 An endogenous undefined biochemical factorAn endogenous undefined biochemical factor
can induce undifferentiated peritoneal cells tocan induce undifferentiated peritoneal cells to
develop into endometrial tissue.develop into endometrial tissue.
6.6. Stem cell may be a sourceStem cell may be a source
7.7. Activation of mullerian cell restActivation of mullerian cell rest
Factor with increase risk of endometriosisFactor with increase risk of endometriosis
 In fertilityIn fertility – when 3 groups of patients were compared i.e.– when 3 groups of patients were compared i.e.
• Asymptomatic patients under going an unrelated procedureAsymptomatic patients under going an unrelated procedure
• Symptomatic patientsSymptomatic patients
• In fertile patientsIn fertile patients
• Highest prevalence rate are typically found in infertile patientsHighest prevalence rate are typically found in infertile patients
ranging from 5-50%.ranging from 5-50%.
 Red hair colourRed hair colour – Direct correlation– Direct correlation
 Early age at menarcheEarly age at menarche
 Shorter menstrual cycleShorter menstrual cycle
 Hypermenorrhoea / menorrhagiaHypermenorrhoea / menorrhagia
 NulliparityNulliparity
 Mullerian anomalies – obstructive and non obstructive –Mullerian anomalies – obstructive and non obstructive –
higher incidence in patients with septate or arcuate uterushigher incidence in patients with septate or arcuate uterus
 High social classHigh social class
 One of multiple fetal gestationOne of multiple fetal gestation – Due to higher estrogen– Due to higher estrogen
exposureexposure
 DES exposure in uteroDES exposure in utero – DES alter estrogen receptor– DES alter estrogen receptor
expression and immune system.expression and immune system.
Endometriosis in first degree relativeEndometriosis in first degree relative
SITES OF ENDOMETRIOSIS
Sites of EndometriosisSites of Endometriosis
 Pelvis –Pelvis –
• OvariesOvaries
• Pouch of DouglasPouch of Douglas
• Uterosacral ligamentUterosacral ligament
• Broad ligament and round ligamentBroad ligament and round ligament
• Recto vaginal septumRecto vaginal septum
• Fallopian tubesFallopian tubes
• The back of the uterus and posterior cul-de-sacThe back of the uterus and posterior cul-de-sac
• The front of the uterus and the anterior cul-de-sacThe front of the uterus and the anterior cul-de-sac
• Pelvic and back wallPelvic and back wall
TUBAL ENDOMETRIOSIS
 Extra genital / Extra pelvic –Extra genital / Extra pelvic –
• Most common sites of extra pelvic disease is gastro intestinal –Most common sites of extra pelvic disease is gastro intestinal –
rectosigmoid, appendix, small bowel, rectumrectosigmoid, appendix, small bowel, rectum
• Urinary tract – ratio of bladder : ureter : kidney is 40:5:1Urinary tract – ratio of bladder : ureter : kidney is 40:5:1
• Diaphragmatic or thoracicDiaphragmatic or thoracic
• LiverLiver
• The only site where extra genital endometriosis has not beenThe only site where extra genital endometriosis has not been
reported is spleenreported is spleen
 Other rarer sites –Other rarer sites –
• Described in virtually every location that can be reached byDescribed in virtually every location that can be reached by
hematogenous, lymphatic or direct disseminationhematogenous, lymphatic or direct dissemination
• HepaticHepatic
• CutaneousCutaneous
• MusculoskeletalMusculoskeletal
• Nerve – commonly in sciatic nerveNerve – commonly in sciatic nerve
• Surgical scarsSurgical scars
• CervicalCervical
• BrainBrain
• EyesEyes
SUBDIAPHRAGMATIC
ENDOMETRIOSIS
LUNG
ENDOMETRIOSIS
LUNG ENDOMETRIOSIS
Endometriosis and InfertilityEndometriosis and Infertility
 Numerous mechanisms :Numerous mechanisms :
• Decreased tuboovarian motilityDecreased tuboovarian motility
• Ovulatory dysfunctionOvulatory dysfunction
 AnavulationAnavulation
 Impaired follicle growthImpaired follicle growth
• Luteal insufficiencyLuteal insufficiency
 Decreased circulatory EDecreased circulatory E22 and progesteroneand progesterone
• Luteinized unruptured follicle syndromeLuteinized unruptured follicle syndrome
• Intraperitoneal inflammationIntraperitoneal inflammation
• Disturbed LH surgeDisturbed LH surge
• Decreased fertilizationDecreased fertilization
• Decreased implantation rateDecreased implantation rate
• Deleterious effect on sperm motilityDeleterious effect on sperm motility
• Decreased “Spontaneous Monthly Fecundity Rate”Decreased “Spontaneous Monthly Fecundity Rate”
(MFR)(MFR)
DIAGNOSIS OF ENDOMETRIOSISDIAGNOSIS OF ENDOMETRIOSIS
History Examination BBT
or
Benzamine sign
Investigation
Non invasive
Blood
investigations
or
Serum markers
Imaging
|
USG
MRI
TVS
TRUS
Invasive
Laparoscopy
+
Histology
Laparotomy
SYMPTOMATOLOGYSYMPTOMATOLOGY
 Pelvic painPelvic pain
• Dysmenorrhea – Especially suggestive of endometriosisDysmenorrhea – Especially suggestive of endometriosis
if it occurs after years of pain free menstruation.if it occurs after years of pain free menstruation.
Start before onset of menstruation and continuesStart before onset of menstruation and continues
Usually bilateralUsually bilateral
• Deep dyspareuniaDeep dyspareunia
• Chronic pelvic painChronic pelvic pain
• Ovualtion painOvualtion pain
• Other types of pain – SciaticaOther types of pain – Sciatica
 InfertilityInfertility
 Symptoms of extra pelvic endometriosis- typically presentSymptoms of extra pelvic endometriosis- typically present
cyclicaly, correlated with menstruation so-calledcyclicaly, correlated with menstruation so-called catamenialcatamenial
symptomssymptoms which are considered pathognomonic. Later inwhich are considered pathognomonic. Later in
disease progression, symptoms become more continuous.disease progression, symptoms become more continuous.
 GI symptom :-GI symptom :-
• DiarrhoeaDiarrhoea
• ConstipationConstipation
• TenesmusTenesmus
• Abdominal distensionAbdominal distension
• Bowel obstruction –Bowel obstruction –
In more advanceIn more advance
disease & perforationdisease & perforation
• Urinary Symptom:
– Hematuria
– Dysuria
– Backache
Diaphragmatic and
thoracic symptoms
 Other symptoms
– Cyclical Sciatica
– Catamenial seizure
– Chronic fatigue
– Mood swing
– Intermittent pyrexia
(Benjamin sign)
EXAMINATIONEXAMINATION
INSPECTION:INSPECTION: Scar endometriosisScar endometriosis
PER SPECULUM EXAMINATION:PER SPECULUM EXAMINATION: Cervical endometriosisCervical endometriosis
BIMANUAL EXAMINATION:BIMANUAL EXAMINATION:
 Focal tendernessFocal tenderness
 Lateral cervical displacementLateral cervical displacement
 Fixed retroverted uterusFixed retroverted uterus
 Uterosacral / cul-de-sac nodularityUterosacral / cul-de-sac nodularity
 Painful swelling of rectovaginal septumPainful swelling of rectovaginal septum
 Unilateral cystic ovarian enlargementUnilateral cystic ovarian enlargement
 ↓↓ mobility of fallopian tubes / ovariesmobility of fallopian tubes / ovaries
““Deeply infiltrating nodules are most reliably detected whenDeeply infiltrating nodules are most reliably detected when
clinical examination is performed during menstruation”clinical examination is performed during menstruation”
(Evidence level III, RCOG Guideline No. 24, 2006).(Evidence level III, RCOG Guideline No. 24, 2006).
 THE BENJAMIN SIGNTHE BENJAMIN SIGN::
When Basal BodyWhen Basal Body
Temperature (BBT) of anTemperature (BBT) of an
adolescent girl, with anadolescent girl, with an
endometriotic syndrome,endometriotic syndrome,
stays high during thestays high during the
menstrual flow or hasmenstrual flow or has upup
and downsand downs during theduring the
same and falls onlysame and falls only at theat the
end of it, we shouldend of it, we should
strongly suspectstrongly suspect
endometriosis and go forendometriosis and go for
a laparoscopy.a laparoscopy.
37,5
37,4
37,3 
37,2  
37,1    
37     
36.9  
36,8 
36,7
36,6
36,5
Menstruación
Atypical Benjamin
sign
Invasive procedures should not be used in adolescents withInvasive procedures should not be used in adolescents with
severe dysmenorrhea if their basal body temperature, thesevere dysmenorrhea if their basal body temperature, the
so called “so called “Benjamin signBenjamin sign”, has not been investigated.”, has not been investigated.
 BBT is charted fromBBT is charted from
22 day of the cycle22 day of the cycle
to end of flow for atto end of flow for at
least 2cycle. Thereleast 2cycle. There
is a late decline ofis a late decline of
BBT after the onsetBBT after the onset
of menstruation inof menstruation in
34.5% of cases.34.5% of cases.
Markers for endometriosisMarkers for endometriosis No blood test is reliable for the diagnosis ofNo blood test is reliable for the diagnosis of
endometriosisendometriosis
Tumour markers and polypeptidesTumour markers and polypeptides
 CA-125, CA-19-9CA-125, CA-19-9
Immunological markersImmunological markers
 Cytokines: IL-6, TNFCytokines: IL-6, TNF
 AutoantibodiesAutoantibodies
(1) Antiendometrial: Serum & Peritoneal fluid(1) Antiendometrial: Serum & Peritoneal fluid
(2) Autoantibodies to markers of oxidative stress(2) Autoantibodies to markers of oxidative stress
ULTRASONOGRAPHYULTRASONOGRAPHY
 Limited utilityLimited utility
 Lacks adequate resolution to identify superficialLacks adequate resolution to identify superficial
peritoneal implants,peritoneal implants, small (<2 cm) ovariansmall (<2 cm) ovarian
endometriomata and adhesionsendometriomata and adhesions
TVSTVS
 Help in the diagnosis of endometriomas, bladder lesions,Help in the diagnosis of endometriomas, bladder lesions,
deep nodules e.g. on rectovaginal septumdeep nodules e.g. on rectovaginal septum
TRUSTRUS
Demonstrate rectovaginalDemonstrate rectovaginal
septum involvement &septum involvement &
posterior bladder betterposterior bladder better
than MRIthan MRI
Sensitivity- 97%Sensitivity- 97%
Specificity- 96%Specificity- 96%
(ESHRE guideline)(ESHRE guideline)
CT - ScanCT - Scan
• Endometriomas mayEndometriomas may
appear solid, cystic orappear solid, cystic or
mixedmixed
• Because of poorBecause of poor
specificity & highspecificity & high
radiation, CT has beenradiation, CT has been
replaced by MRIreplaced by MRI
MRIMRI
 Use full in deep pelvic endometriosisUse full in deep pelvic endometriosis
 Magnetic resonance imaging using fat saturation canMagnetic resonance imaging using fat saturation can
detect up to 50% of small, haemorrhagic lesionsdetect up to 50% of small, haemorrhagic lesions
measuring not more than 5 mm and allows thenmeasuring not more than 5 mm and allows then
diagnose of mild disease in 75% of cases.diagnose of mild disease in 75% of cases.
LAPAROSCOPY
LAPAROSCOPYLAPAROSCOPY
 For definitive diagnosis of endometriosis visualFor definitive diagnosis of endometriosis visual
inspection of the pelvis at laparoscopy is goldinspection of the pelvis at laparoscopy is gold
standard, unless disease is visible in vagina orstandard, unless disease is visible in vagina or
elsewhereelsewhere
 Should not be performed during or within 3Should not be performed during or within 3
months of hormonal treatment to avoid undermonths of hormonal treatment to avoid under
diagnosisdiagnosis
Types of lesionTypes of lesion
 Three primary types of endometriosis areThree primary types of endometriosis are
• Superficial peritoneal lesion,Superficial peritoneal lesion,
• Ovarian endometriomaOvarian endometrioma
• Deep infiltrating endometriosisDeep infiltrating endometriosis
Superficial peritoneal lesionSuperficial peritoneal lesion
 Typically located on pelvic organ or pelvicTypically located on pelvic organ or pelvic
peritoneumperitoneum
 Classical lesion are ‘Classical lesion are ‘powder burn or gun shotpowder burn or gun shot
lesionlesion.’ These are black, dark brown or bluish.’ These are black, dark brown or bluish
nodules or small cyst containing old hemorrhage.nodules or small cyst containing old hemorrhage.
 May be associated with hemosiderin depositMay be associated with hemosiderin deposit
 Non classical lesion are subtle lesions – RedNon classical lesion are subtle lesions – Red
implantsimplants
(Petechial/vasicular/polypoidal/hemorrhage/ red(Petechial/vasicular/polypoidal/hemorrhage/ red
flame like.flame like.
 Serous or clear vesiclesSerous or clear vesicles
 White plaquesScaringWhite plaquesScaring
 Yellow-brown discoloration of the peritoneumYellow-brown discoloration of the peritoneum
 Sub ovarian adhesionSub ovarian adhesion
Variety of endometriotic lesions seen at laparoscopy
Endometrioma (Chocolate cyst)Endometrioma (Chocolate cyst)
 Usually located onUsually located on
anterior surface of theanterior surface of the
ovaryovary
 Diameter <Diameter < 12cm12cm
 Associated with retractionAssociated with retraction
pigmentation andpigmentation and
adhesion to posterioradhesion to posterior
peritoneumperitoneum
Endometrioma(Chocolate cyst)Endometrioma(Chocolate cyst)
 Contain tarry,thickContain tarry,thick
chocolate coloured fluidchocolate coloured fluid
composed of hemosiderincomposed of hemosiderin
derived from previousderived from previous
intraovarian hemorrhageintraovarian hemorrhage
 Marker of more extensiveMarker of more extensive
pelvic and intestinalpelvic and intestinal
diseasedisease
 Histological conformationHistological conformation
is necessaryis necessary
CLASSIFICATIONCLASSIFICATION
 Current classification is by “American society ofCurrent classification is by “American society of
Reproductive Medicine”Reproductive Medicine”, former “American, former “American
Fertility Society”(AFS) systemFertility Society”(AFS) system
 Based on morphology, size and depth ofBased on morphology, size and depth of
peritoneal implantperitoneal implant
 Morphology-Morphology-
Red ( Red, Red-pink & clear lesions)Red ( Red, Red-pink & clear lesions)
White (White, yellow-brown & peritoneal defects)White (White, yellow-brown & peritoneal defects)
Black (Black & blue lesions)Black (Black & blue lesions)
 Presence extent and type of peritonealPresence extent and type of peritoneal
adhesionsadhesions
 Degree of cul-de-sac obliterationDegree of cul-de-sac obliteration
Staging
– American society of Reproductive
Medicine, 1996
Stage I – Minimal
Isolated superficial implants,
No adhesions
Stage II – Mild
More superficial implants (<5cm),
No significant adhesions
Stage III – Moderate
Multiple superficial & invasive implants,
Peritubal & Periovarian adhesions may be
present
Stage IV – Severe
Multiple implants,
Ovarian endometriomas,
Many dense adhesions
TREATMENTTREATMENT
 Must be individualizedMust be individualized
 Highly dependent on the wishes of the patient -Highly dependent on the wishes of the patient -
fertility or contraceptionfertility or contraception
 Symptom and severity of the diseaseSymptom and severity of the disease
 Location of the diseaseLocation of the disease
MEDICAL TREATMENTMEDICAL TREATMENT
 Four chief medical approaches-Four chief medical approaches-
1- Analgesia1- Analgesia
2- Suppresion of ovulatory function2- Suppresion of ovulatory function
3- Direct action of endometrial implant3- Direct action of endometrial implant
4- Modulation of immune system4- Modulation of immune system
 Non Hormonal MedicationsNon Hormonal Medications
 NSAIDs :NSAIDs : NaproxenNaproxen
• Mechanism:Mechanism: Local anti-nocioceptive effectLocal anti-nocioceptive effect
↓↓ central sensitizationcentral sensitization
Anti-inflammatory effectsAnti-inflammatory effects
• Side effects:Side effects: Gastric ulcerationsGastric ulcerations
Inhibition of ovulationInhibition of ovulation
““Inconclusive evidence regarding their effectivenessInconclusive evidence regarding their effectiveness
(especially Naproxen)”(especially Naproxen)” ((ESHRE, 2007 updateESHRE, 2007 update))
Antiangiogenic-Antiangiogenic-
 StatinsStatins
 ThalidomideThalidomide
 Inhibition of MMPs : ProgesteroneInhibition of MMPs : Progesterone
 Anti VEGF antibodiesAnti VEGF antibodies
 Angiostatic agents (TNP470, endostatin,Angiostatic agents (TNP470, endostatin,
rapamycin)rapamycin)
Table 1. Medical treatment options in women with symptomatic endometriosis who are not
seeking pregnancy.
First-line treatments
Peritoneal disease and endometriotic cysts 3 cm
Oestrogeneprogestin combinations used cyclically or continuously* (oral,
intravaginal or transdermic use)
Rectovaginal lesions-
Noretistherone acetate, 2.5 mg/day per os used continuously*
Second-line treatments
Depot GnRH analogues plus add-back therapy (e.g. tibolone 2.5 mg/day per os)
Alternative progestins (e.g. medroxyprogesterone acetate, desogestrel,
cyproterone acetate)
Third-line treatments
Low-dose danazol (e.g. 200 mg/day, oral or intravaginal use)
Gestrinone, 2.5 mg twice weekly per os
Specific conditions
Parous women with dysmenorrhoea as main symptom
Levonorgestrel-releasing intra-uterine device
Hysterectomized women with residual disease
Depot medroxyprogesterone acetate (150 mg intramuscularly every 3e6 months)
GnRH, gonadotrophin-releasing hormone.
* A 7-day interruption is suggested in case of breakthrough bleeding during
SURGICAL TREATMENTSURGICAL TREATMENT
GoalGoal
 To excise all visible lesions and associated adhesionsTo excise all visible lesions and associated adhesions
 To restore normal anatomyTo restore normal anatomy
 Laparoscopy is betterLaparoscopy is better
 Laparotomy – reserve forLaparotomy – reserve for
• Advanced stage diseaseAdvanced stage disease
• Who cannot go laparoscopyWho cannot go laparoscopy
• Fertility is not desiredFertility is not desired
Laparoscopic ManagementLaparoscopic Management
LAPAROTOMYLAPAROTOMY
LAPAROTOMYLAPAROTOMY
 Total abdominal hysterectomy + bilateral salpingo-Total abdominal hysterectomy + bilateral salpingo-
oophrectomyoophrectomy
 Hysterectomy alone is not effectiveHysterectomy alone is not effective
• Reserve for severe situationReserve for severe situation
• HRT is recommended in young women afterHRT is recommended in young women after
bilateral oophorectomy (bilateral oophorectomy (ROCG guideline 24, 2006).ROCG guideline 24, 2006).
• Estrogen should be withheld until 3 month afterEstrogen should be withheld until 3 month after
surgerysurgery
Empirical treatment of pain symptomsEmpirical treatment of pain symptoms
without a definitive Diagnosiswithout a definitive Diagnosis
 CounsellingCounselling
 Adequate analgesiaAdequate analgesia
 Nutritional therapyNutritional therapy
 ProgestagensProgestagens
 Combined oral contraceptive (COC)Combined oral contraceptive (COC)
Treatment of endometriosis-associatedTreatment of endometriosis-associated
pain in confirmed diseasepain in confirmed disease
 Non-steroidal anti-inflammatory drugsNon-steroidal anti-inflammatory drugs
 Hormonal treatmentHormonal treatment
 Surgical treatmentSurgical treatment
Infertility &
Suspected endometriosis
Operative Laparoscopy
Watchful waitingSuccessPregnancy Failure
AssistedAssisted
ReproductionReproduction
TREATMENT PROTOCOL FOR
ENDOMETRIOSIS ASSOCIATED INFERTILITY
Endometriosis by Dr syeda komal

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Endometriosis by Dr syeda komal

  • 1.
  • 3.  Endometriosis is a disease or better a syndromeEndometriosis is a disease or better a syndrome that starts around the prepubertal age,that starts around the prepubertal age, flourishing after menarche, with symptomsflourishing after menarche, with symptoms progressing in intensity through the years.progressing in intensity through the years.  Predominantly found in women of reproductivePredominantly found in women of reproductive ageage  Found in all the ethnic & social groupsFound in all the ethnic & social groups
  • 4. DEFINITIONDEFINITION  EndometriosisEndometriosis (from(from endoendo, "inside", and, "inside", and metrametra, ", "wombwomb""  Presence of endometrial like tissue (glands/stroma)Presence of endometrial like tissue (glands/stroma) outside the uterus which induces chronic inflammatoryoutside the uterus which induces chronic inflammatory reaction.reaction.  Most frequent sites are pelvic viscera & peritoneum outMost frequent sites are pelvic viscera & peritoneum out of which most common site is ovary (RCOG guidelineof which most common site is ovary (RCOG guideline no. 24, 2006)no. 24, 2006)  Adenomyosis is ectopic endometrium inside theAdenomyosis is ectopic endometrium inside the myometrium of uterus, previously known asmyometrium of uterus, previously known as endometriosis interna.endometriosis interna.
  • 5. INCIDENCEINCIDENCE • Asymptomatic women undergoing tubal sterilizationAsymptomatic women undergoing tubal sterilization i.e. women with proven fertility - 7%i.e. women with proven fertility - 7% • Primary infertility (20-30%)Primary infertility (20-30%) • Dysmenorrhoea (40-60%)Dysmenorrhoea (40-60%) • Chronic pelvic pain(71-80%)Chronic pelvic pain(71-80%)
  • 6. ETIOLOGYETIOLOGY  Exact etiology of endometriosis is unknown.Exact etiology of endometriosis is unknown.  Understanding of endometriosis is just a beginning.Understanding of endometriosis is just a beginning.  It is a estrogen dependent disease.It is a estrogen dependent disease.
  • 7. HYPOTHESISHYPOTHESIS 1.1. Retrograde menstruation/ectopic transplantation/Retrograde menstruation/ectopic transplantation/ Sampson’s theory –Sampson’s theory – (Lancet, 2004
  • 8. • Most widely recognized & plausible theory on the genesisMost widely recognized & plausible theory on the genesis of endometriosis.of endometriosis. • Based on the assumption that endometriosis is causedBased on the assumption that endometriosis is caused by the seeding or implantation of endometrial cell byby the seeding or implantation of endometrial cell by trans tubal regurgitation during menstruation.trans tubal regurgitation during menstruation. • Supported by – Blood can be found in peritoneal cavitySupported by – Blood can be found in peritoneal cavity on laparoscopy during menstruation in 75-90%on laparoscopy during menstruation in 75-90% - most often found in dependent portions- most often found in dependent portions of the pelvis like ovaries, anterior & posterior cul-de-sac,of the pelvis like ovaries, anterior & posterior cul-de-sac, the uterosacral ligaments, posterior uterus, posteriorthe uterosacral ligaments, posterior uterus, posterior broad ligaments.broad ligaments.  More in women with stenosis of internal osMore in women with stenosis of internal os  Mullerian abnormalitiesMullerian abnormalities
  • 9. 2.2. Coelomic Metaplasia/ MetaplasticCoelomic Metaplasia/ Metaplastic Transformation/ Meyer’s theoryTransformation/ Meyer’s theory --  Both peritoneal and endometrial tissues share aBoth peritoneal and endometrial tissues share a common embryologic precursor the coelomic cell.common embryologic precursor the coelomic cell.  Metaplastic transformation of coelomic epitheliumMetaplastic transformation of coelomic epithelium into endometrial tissue can occur.into endometrial tissue can occur.  Premenarchal girl who have never menstruatedPremenarchal girl who have never menstruated  Unusual sites( Extremities, brain, pleura)Unusual sites( Extremities, brain, pleura)
  • 10. 33. Lymphatic or Hematogenous Spread Distant to. Lymphatic or Hematogenous Spread Distant to pelvis/ Hallban’s theory –pelvis/ Hallban’s theory –  Explain the observation of endometriosis in unusualExplain the observation of endometriosis in unusual sites such as brain & pleurasites such as brain & pleura  Extra pelvic endometriosis - vascular or lymphaticExtra pelvic endometriosis - vascular or lymphatic dissemination of endometrial cellsdissemination of endometrial cells  Ovarian endometriotic lesion may arise directly fromOvarian endometriotic lesion may arise directly from ovarian surface epithelium through a metaplasticovarian surface epithelium through a metaplastic differentiation process induced by activation of andifferentiation process induced by activation of an oncogenic K-ras allele.oncogenic K-ras allele.  Ovarian endometriosis - retrograde menstruation orOvarian endometriosis - retrograde menstruation or lymphatic flow from the uterus.lymphatic flow from the uterus.
  • 11. 4.4. Direct Transplantation from Tissue Trauma orDirect Transplantation from Tissue Trauma or SurgerySurgery  Explain the finding of localized endometriosisExplain the finding of localized endometriosis cesarean-section scar or episiotomy sites.cesarean-section scar or episiotomy sites. • Biologically distinct tissue may directly attach to aBiologically distinct tissue may directly attach to a site accompanied by initiation of localized oncogenic-site accompanied by initiation of localized oncogenic- like cascades leading to implant survival.like cascades leading to implant survival. • Decreased immunosurveillance which wouldDecreased immunosurveillance which would normally clear the ectopic tissue--may also be therenormally clear the ectopic tissue--may also be there
  • 12. 5.5. Induction theory –Induction theory –  An endogenous undefined biochemical factorAn endogenous undefined biochemical factor can induce undifferentiated peritoneal cells tocan induce undifferentiated peritoneal cells to develop into endometrial tissue.develop into endometrial tissue. 6.6. Stem cell may be a sourceStem cell may be a source 7.7. Activation of mullerian cell restActivation of mullerian cell rest
  • 13. Factor with increase risk of endometriosisFactor with increase risk of endometriosis  In fertilityIn fertility – when 3 groups of patients were compared i.e.– when 3 groups of patients were compared i.e. • Asymptomatic patients under going an unrelated procedureAsymptomatic patients under going an unrelated procedure • Symptomatic patientsSymptomatic patients • In fertile patientsIn fertile patients • Highest prevalence rate are typically found in infertile patientsHighest prevalence rate are typically found in infertile patients ranging from 5-50%.ranging from 5-50%.  Red hair colourRed hair colour – Direct correlation– Direct correlation  Early age at menarcheEarly age at menarche  Shorter menstrual cycleShorter menstrual cycle  Hypermenorrhoea / menorrhagiaHypermenorrhoea / menorrhagia  NulliparityNulliparity
  • 14.  Mullerian anomalies – obstructive and non obstructive –Mullerian anomalies – obstructive and non obstructive – higher incidence in patients with septate or arcuate uterushigher incidence in patients with septate or arcuate uterus  High social classHigh social class  One of multiple fetal gestationOne of multiple fetal gestation – Due to higher estrogen– Due to higher estrogen exposureexposure  DES exposure in uteroDES exposure in utero – DES alter estrogen receptor– DES alter estrogen receptor expression and immune system.expression and immune system. Endometriosis in first degree relativeEndometriosis in first degree relative
  • 16. Sites of EndometriosisSites of Endometriosis  Pelvis –Pelvis – • OvariesOvaries • Pouch of DouglasPouch of Douglas • Uterosacral ligamentUterosacral ligament • Broad ligament and round ligamentBroad ligament and round ligament • Recto vaginal septumRecto vaginal septum • Fallopian tubesFallopian tubes • The back of the uterus and posterior cul-de-sacThe back of the uterus and posterior cul-de-sac • The front of the uterus and the anterior cul-de-sacThe front of the uterus and the anterior cul-de-sac • Pelvic and back wallPelvic and back wall
  • 18.  Extra genital / Extra pelvic –Extra genital / Extra pelvic – • Most common sites of extra pelvic disease is gastro intestinal –Most common sites of extra pelvic disease is gastro intestinal – rectosigmoid, appendix, small bowel, rectumrectosigmoid, appendix, small bowel, rectum • Urinary tract – ratio of bladder : ureter : kidney is 40:5:1Urinary tract – ratio of bladder : ureter : kidney is 40:5:1 • Diaphragmatic or thoracicDiaphragmatic or thoracic • LiverLiver • The only site where extra genital endometriosis has not beenThe only site where extra genital endometriosis has not been reported is spleenreported is spleen  Other rarer sites –Other rarer sites – • Described in virtually every location that can be reached byDescribed in virtually every location that can be reached by hematogenous, lymphatic or direct disseminationhematogenous, lymphatic or direct dissemination • HepaticHepatic • CutaneousCutaneous • MusculoskeletalMusculoskeletal • Nerve – commonly in sciatic nerveNerve – commonly in sciatic nerve • Surgical scarsSurgical scars • CervicalCervical • BrainBrain • EyesEyes
  • 21. Endometriosis and InfertilityEndometriosis and Infertility  Numerous mechanisms :Numerous mechanisms : • Decreased tuboovarian motilityDecreased tuboovarian motility • Ovulatory dysfunctionOvulatory dysfunction  AnavulationAnavulation  Impaired follicle growthImpaired follicle growth • Luteal insufficiencyLuteal insufficiency  Decreased circulatory EDecreased circulatory E22 and progesteroneand progesterone • Luteinized unruptured follicle syndromeLuteinized unruptured follicle syndrome • Intraperitoneal inflammationIntraperitoneal inflammation • Disturbed LH surgeDisturbed LH surge • Decreased fertilizationDecreased fertilization • Decreased implantation rateDecreased implantation rate • Deleterious effect on sperm motilityDeleterious effect on sperm motility • Decreased “Spontaneous Monthly Fecundity Rate”Decreased “Spontaneous Monthly Fecundity Rate” (MFR)(MFR)
  • 22. DIAGNOSIS OF ENDOMETRIOSISDIAGNOSIS OF ENDOMETRIOSIS History Examination BBT or Benzamine sign Investigation Non invasive Blood investigations or Serum markers Imaging | USG MRI TVS TRUS Invasive Laparoscopy + Histology Laparotomy
  • 23. SYMPTOMATOLOGYSYMPTOMATOLOGY  Pelvic painPelvic pain • Dysmenorrhea – Especially suggestive of endometriosisDysmenorrhea – Especially suggestive of endometriosis if it occurs after years of pain free menstruation.if it occurs after years of pain free menstruation. Start before onset of menstruation and continuesStart before onset of menstruation and continues Usually bilateralUsually bilateral • Deep dyspareuniaDeep dyspareunia • Chronic pelvic painChronic pelvic pain • Ovualtion painOvualtion pain • Other types of pain – SciaticaOther types of pain – Sciatica  InfertilityInfertility  Symptoms of extra pelvic endometriosis- typically presentSymptoms of extra pelvic endometriosis- typically present cyclicaly, correlated with menstruation so-calledcyclicaly, correlated with menstruation so-called catamenialcatamenial symptomssymptoms which are considered pathognomonic. Later inwhich are considered pathognomonic. Later in disease progression, symptoms become more continuous.disease progression, symptoms become more continuous.
  • 24.  GI symptom :-GI symptom :- • DiarrhoeaDiarrhoea • ConstipationConstipation • TenesmusTenesmus • Abdominal distensionAbdominal distension • Bowel obstruction –Bowel obstruction – In more advanceIn more advance disease & perforationdisease & perforation • Urinary Symptom: – Hematuria – Dysuria – Backache
  • 25. Diaphragmatic and thoracic symptoms  Other symptoms – Cyclical Sciatica – Catamenial seizure – Chronic fatigue – Mood swing – Intermittent pyrexia (Benjamin sign)
  • 26. EXAMINATIONEXAMINATION INSPECTION:INSPECTION: Scar endometriosisScar endometriosis PER SPECULUM EXAMINATION:PER SPECULUM EXAMINATION: Cervical endometriosisCervical endometriosis BIMANUAL EXAMINATION:BIMANUAL EXAMINATION:  Focal tendernessFocal tenderness  Lateral cervical displacementLateral cervical displacement  Fixed retroverted uterusFixed retroverted uterus  Uterosacral / cul-de-sac nodularityUterosacral / cul-de-sac nodularity  Painful swelling of rectovaginal septumPainful swelling of rectovaginal septum  Unilateral cystic ovarian enlargementUnilateral cystic ovarian enlargement  ↓↓ mobility of fallopian tubes / ovariesmobility of fallopian tubes / ovaries ““Deeply infiltrating nodules are most reliably detected whenDeeply infiltrating nodules are most reliably detected when clinical examination is performed during menstruation”clinical examination is performed during menstruation” (Evidence level III, RCOG Guideline No. 24, 2006).(Evidence level III, RCOG Guideline No. 24, 2006).
  • 27.  THE BENJAMIN SIGNTHE BENJAMIN SIGN:: When Basal BodyWhen Basal Body Temperature (BBT) of anTemperature (BBT) of an adolescent girl, with anadolescent girl, with an endometriotic syndrome,endometriotic syndrome, stays high during thestays high during the menstrual flow or hasmenstrual flow or has upup and downsand downs during theduring the same and falls onlysame and falls only at theat the end of it, we shouldend of it, we should strongly suspectstrongly suspect endometriosis and go forendometriosis and go for a laparoscopy.a laparoscopy. 37,5 37,4 37,3  37,2   37,1     37      36.9   36,8  36,7 36,6 36,5 Menstruación Atypical Benjamin sign
  • 28. Invasive procedures should not be used in adolescents withInvasive procedures should not be used in adolescents with severe dysmenorrhea if their basal body temperature, thesevere dysmenorrhea if their basal body temperature, the so called “so called “Benjamin signBenjamin sign”, has not been investigated.”, has not been investigated.  BBT is charted fromBBT is charted from 22 day of the cycle22 day of the cycle to end of flow for atto end of flow for at least 2cycle. Thereleast 2cycle. There is a late decline ofis a late decline of BBT after the onsetBBT after the onset of menstruation inof menstruation in 34.5% of cases.34.5% of cases.
  • 29. Markers for endometriosisMarkers for endometriosis No blood test is reliable for the diagnosis ofNo blood test is reliable for the diagnosis of endometriosisendometriosis Tumour markers and polypeptidesTumour markers and polypeptides  CA-125, CA-19-9CA-125, CA-19-9 Immunological markersImmunological markers  Cytokines: IL-6, TNFCytokines: IL-6, TNF  AutoantibodiesAutoantibodies (1) Antiendometrial: Serum & Peritoneal fluid(1) Antiendometrial: Serum & Peritoneal fluid (2) Autoantibodies to markers of oxidative stress(2) Autoantibodies to markers of oxidative stress
  • 30. ULTRASONOGRAPHYULTRASONOGRAPHY  Limited utilityLimited utility  Lacks adequate resolution to identify superficialLacks adequate resolution to identify superficial peritoneal implants,peritoneal implants, small (<2 cm) ovariansmall (<2 cm) ovarian endometriomata and adhesionsendometriomata and adhesions TVSTVS  Help in the diagnosis of endometriomas, bladder lesions,Help in the diagnosis of endometriomas, bladder lesions, deep nodules e.g. on rectovaginal septumdeep nodules e.g. on rectovaginal septum
  • 31. TRUSTRUS Demonstrate rectovaginalDemonstrate rectovaginal septum involvement &septum involvement & posterior bladder betterposterior bladder better than MRIthan MRI Sensitivity- 97%Sensitivity- 97% Specificity- 96%Specificity- 96% (ESHRE guideline)(ESHRE guideline)
  • 32. CT - ScanCT - Scan • Endometriomas mayEndometriomas may appear solid, cystic orappear solid, cystic or mixedmixed • Because of poorBecause of poor specificity & highspecificity & high radiation, CT has beenradiation, CT has been replaced by MRIreplaced by MRI
  • 33. MRIMRI  Use full in deep pelvic endometriosisUse full in deep pelvic endometriosis  Magnetic resonance imaging using fat saturation canMagnetic resonance imaging using fat saturation can detect up to 50% of small, haemorrhagic lesionsdetect up to 50% of small, haemorrhagic lesions measuring not more than 5 mm and allows thenmeasuring not more than 5 mm and allows then diagnose of mild disease in 75% of cases.diagnose of mild disease in 75% of cases.
  • 35. LAPAROSCOPYLAPAROSCOPY  For definitive diagnosis of endometriosis visualFor definitive diagnosis of endometriosis visual inspection of the pelvis at laparoscopy is goldinspection of the pelvis at laparoscopy is gold standard, unless disease is visible in vagina orstandard, unless disease is visible in vagina or elsewhereelsewhere  Should not be performed during or within 3Should not be performed during or within 3 months of hormonal treatment to avoid undermonths of hormonal treatment to avoid under diagnosisdiagnosis
  • 36. Types of lesionTypes of lesion  Three primary types of endometriosis areThree primary types of endometriosis are • Superficial peritoneal lesion,Superficial peritoneal lesion, • Ovarian endometriomaOvarian endometrioma • Deep infiltrating endometriosisDeep infiltrating endometriosis
  • 37. Superficial peritoneal lesionSuperficial peritoneal lesion  Typically located on pelvic organ or pelvicTypically located on pelvic organ or pelvic peritoneumperitoneum  Classical lesion are ‘Classical lesion are ‘powder burn or gun shotpowder burn or gun shot lesionlesion.’ These are black, dark brown or bluish.’ These are black, dark brown or bluish nodules or small cyst containing old hemorrhage.nodules or small cyst containing old hemorrhage.  May be associated with hemosiderin depositMay be associated with hemosiderin deposit  Non classical lesion are subtle lesions – RedNon classical lesion are subtle lesions – Red implantsimplants (Petechial/vasicular/polypoidal/hemorrhage/ red(Petechial/vasicular/polypoidal/hemorrhage/ red flame like.flame like.  Serous or clear vesiclesSerous or clear vesicles  White plaquesScaringWhite plaquesScaring  Yellow-brown discoloration of the peritoneumYellow-brown discoloration of the peritoneum  Sub ovarian adhesionSub ovarian adhesion
  • 38. Variety of endometriotic lesions seen at laparoscopy
  • 39. Endometrioma (Chocolate cyst)Endometrioma (Chocolate cyst)  Usually located onUsually located on anterior surface of theanterior surface of the ovaryovary  Diameter <Diameter < 12cm12cm  Associated with retractionAssociated with retraction pigmentation andpigmentation and adhesion to posterioradhesion to posterior peritoneumperitoneum
  • 40. Endometrioma(Chocolate cyst)Endometrioma(Chocolate cyst)  Contain tarry,thickContain tarry,thick chocolate coloured fluidchocolate coloured fluid composed of hemosiderincomposed of hemosiderin derived from previousderived from previous intraovarian hemorrhageintraovarian hemorrhage  Marker of more extensiveMarker of more extensive pelvic and intestinalpelvic and intestinal diseasedisease  Histological conformationHistological conformation is necessaryis necessary
  • 41. CLASSIFICATIONCLASSIFICATION  Current classification is by “American society ofCurrent classification is by “American society of Reproductive Medicine”Reproductive Medicine”, former “American, former “American Fertility Society”(AFS) systemFertility Society”(AFS) system  Based on morphology, size and depth ofBased on morphology, size and depth of peritoneal implantperitoneal implant  Morphology-Morphology- Red ( Red, Red-pink & clear lesions)Red ( Red, Red-pink & clear lesions) White (White, yellow-brown & peritoneal defects)White (White, yellow-brown & peritoneal defects) Black (Black & blue lesions)Black (Black & blue lesions)  Presence extent and type of peritonealPresence extent and type of peritoneal adhesionsadhesions  Degree of cul-de-sac obliterationDegree of cul-de-sac obliteration
  • 42. Staging – American society of Reproductive Medicine, 1996 Stage I – Minimal Isolated superficial implants, No adhesions Stage II – Mild More superficial implants (<5cm), No significant adhesions
  • 43. Stage III – Moderate Multiple superficial & invasive implants, Peritubal & Periovarian adhesions may be present Stage IV – Severe Multiple implants, Ovarian endometriomas, Many dense adhesions
  • 44. TREATMENTTREATMENT  Must be individualizedMust be individualized  Highly dependent on the wishes of the patient -Highly dependent on the wishes of the patient - fertility or contraceptionfertility or contraception  Symptom and severity of the diseaseSymptom and severity of the disease  Location of the diseaseLocation of the disease
  • 45. MEDICAL TREATMENTMEDICAL TREATMENT  Four chief medical approaches-Four chief medical approaches- 1- Analgesia1- Analgesia 2- Suppresion of ovulatory function2- Suppresion of ovulatory function 3- Direct action of endometrial implant3- Direct action of endometrial implant 4- Modulation of immune system4- Modulation of immune system
  • 46.  Non Hormonal MedicationsNon Hormonal Medications  NSAIDs :NSAIDs : NaproxenNaproxen • Mechanism:Mechanism: Local anti-nocioceptive effectLocal anti-nocioceptive effect ↓↓ central sensitizationcentral sensitization Anti-inflammatory effectsAnti-inflammatory effects • Side effects:Side effects: Gastric ulcerationsGastric ulcerations Inhibition of ovulationInhibition of ovulation ““Inconclusive evidence regarding their effectivenessInconclusive evidence regarding their effectiveness (especially Naproxen)”(especially Naproxen)” ((ESHRE, 2007 updateESHRE, 2007 update))
  • 47. Antiangiogenic-Antiangiogenic-  StatinsStatins  ThalidomideThalidomide  Inhibition of MMPs : ProgesteroneInhibition of MMPs : Progesterone  Anti VEGF antibodiesAnti VEGF antibodies  Angiostatic agents (TNP470, endostatin,Angiostatic agents (TNP470, endostatin, rapamycin)rapamycin)
  • 48. Table 1. Medical treatment options in women with symptomatic endometriosis who are not seeking pregnancy. First-line treatments Peritoneal disease and endometriotic cysts 3 cm Oestrogeneprogestin combinations used cyclically or continuously* (oral, intravaginal or transdermic use) Rectovaginal lesions- Noretistherone acetate, 2.5 mg/day per os used continuously* Second-line treatments Depot GnRH analogues plus add-back therapy (e.g. tibolone 2.5 mg/day per os) Alternative progestins (e.g. medroxyprogesterone acetate, desogestrel, cyproterone acetate) Third-line treatments Low-dose danazol (e.g. 200 mg/day, oral or intravaginal use) Gestrinone, 2.5 mg twice weekly per os Specific conditions Parous women with dysmenorrhoea as main symptom Levonorgestrel-releasing intra-uterine device Hysterectomized women with residual disease Depot medroxyprogesterone acetate (150 mg intramuscularly every 3e6 months) GnRH, gonadotrophin-releasing hormone. * A 7-day interruption is suggested in case of breakthrough bleeding during
  • 49. SURGICAL TREATMENTSURGICAL TREATMENT GoalGoal  To excise all visible lesions and associated adhesionsTo excise all visible lesions and associated adhesions  To restore normal anatomyTo restore normal anatomy  Laparoscopy is betterLaparoscopy is better  Laparotomy – reserve forLaparotomy – reserve for • Advanced stage diseaseAdvanced stage disease • Who cannot go laparoscopyWho cannot go laparoscopy • Fertility is not desiredFertility is not desired
  • 52. LAPAROTOMYLAPAROTOMY  Total abdominal hysterectomy + bilateral salpingo-Total abdominal hysterectomy + bilateral salpingo- oophrectomyoophrectomy  Hysterectomy alone is not effectiveHysterectomy alone is not effective • Reserve for severe situationReserve for severe situation • HRT is recommended in young women afterHRT is recommended in young women after bilateral oophorectomy (bilateral oophorectomy (ROCG guideline 24, 2006).ROCG guideline 24, 2006). • Estrogen should be withheld until 3 month afterEstrogen should be withheld until 3 month after surgerysurgery
  • 53. Empirical treatment of pain symptomsEmpirical treatment of pain symptoms without a definitive Diagnosiswithout a definitive Diagnosis  CounsellingCounselling  Adequate analgesiaAdequate analgesia  Nutritional therapyNutritional therapy  ProgestagensProgestagens  Combined oral contraceptive (COC)Combined oral contraceptive (COC)
  • 54. Treatment of endometriosis-associatedTreatment of endometriosis-associated pain in confirmed diseasepain in confirmed disease  Non-steroidal anti-inflammatory drugsNon-steroidal anti-inflammatory drugs  Hormonal treatmentHormonal treatment  Surgical treatmentSurgical treatment
  • 55. Infertility & Suspected endometriosis Operative Laparoscopy Watchful waitingSuccessPregnancy Failure AssistedAssisted ReproductionReproduction TREATMENT PROTOCOL FOR ENDOMETRIOSIS ASSOCIATED INFERTILITY