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3 : Learning objectives Understand the pathogensis & clinical presentation of endometriosis. Understands consequences associated with endometriosis. Describe various treatment options in the management of endometriosis. Know the surgical principal underlying the conservative and radical approaches to endometriosis surgery. 3
4 : What is endometriosis Presence of ectopic endometrial tissue in extra uterine sites . Endometriosis occurs when the same type of tissue (stroma and glands) that makes up the endometrial lining of the uterus grows on other structures in the pelvis. These cells respond to fluctuations just like those in inside the uterus enlarging and multiplying as the ovaries produce estrogen and progesterone during the menstrual cycle (Garner, 1997). 4
5 : continue Endometriosis is not cancer and there is no cure for it One of the most common diseases but it is also one of the least understood 5
6 : Endometrial tissue Responds to estrogen and progesterone Endometrial tissue is found living outside the uterus If no pregnancy occurs the endometrial lining is shed, the endometrial tissue found outside the uterus breaks down as well causing internal bleeding 6
7 : continue This internal bleeding is absorbed by the surrounding tissue. Over time, implanted tissues grow and form destructive scar tissue and adhesions. collection of blood----- cyst formation rupture, causing excruciating pain 7
8 : Normal pelvic structure 8
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10 : Endometriosis
11 : Where is it found in the body ? (sites of endometriosis) Usually endometriosis is found in the pelvic area It has been found on every pelvic organ, including the uterus (17-55% of women), ovaries (61-78%), tubes, ligaments, ureters, bowel, bladder However, it can be found in anywhere in the body lungs, knees, nose, arms, brain, scar tissue, legs. 11
12 : Endometriosis sites
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14 : Ovarian endometrioma Ovarian chocolate cyst Peritoneal endometrioma Adenomyosis Ovarian endometriosis histology Endometriosis: presence of endometrial glands and stroma outside of the normal location Lung endometriosis 14
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19 : incidence (Refrrences----- dewhursts and evidence based). 8-10 % of reproductive age women. 6% of women under going sterilization 21% being investigated for infertility. 24.5% being investigated for chronic pelvic pain 52% of teenage with CPP syndrome. 19
20 : Is Endometriosis Increasing? Are rates on the rise? changing patterns of menstruation women today have delayed childbirth until their 30s and 40s, meaning they have more periods, which leads to a greater chance for endometrial tissue to migrate through the fallopian tubes greater awareness leads to more diagnosis. environmental toxin dioxin exposure is thought to increase endometriosis occurrences 20
21 : Risk factors Age Most commonly diagnosed in women of reproductive age. more exposure to menstruation shorter cycle/longer duration of flow Single/nulliparous Early menarche Non oral contraception 21
22 : continue Non smoker. Familial association(genetic predisposition) 6-9 times more in ist degree relatives( ch q26, ch20p30) Dysplastic naevus syndrome, melanoma Alcohol, caffeine. PROTECTIONS FACTORS Term pregnancy, regular exercise, smoking, Asian > whites > blacks 22 .
23 : Pathogenesis / etiology Endometriosis is heterogenous not a single disease Exact etiology is not known but there are certain theories. Retrograde menstruation/transplantation Coelomic metaplasia Metastasis Genetic basis Immunologic basis 23
24 : Endometriosis Mechanical Endocrine Immunological Genetic Implantation Metaplasia Endometrial implant Progression & invasion Lymphatic & Blood spread Adapted & Modified from – R.W. Shaw, Gynecology
25 : Retrograde menstruation/transplantation as the primary mechanism involved in the pathogenesis of endometriosis (Lancet, 2004) First described by John Sampson in 1927 25
26 : Lines of evidence supporting Sampson’s Laparoscopy during menses: peritoneal blood can be found in 75-90% of women with patent tubes Peritoneal endometrial cells recovered during menses can attach to and penetrate the peritoneum 26
27 : continue Incidence of endometriosis is increased in women with early menarche, short cycle, menorrhagia or obstructing Mullerian anomalies Commonly found in dependent sites: ovaries, cul-de-sac, U-S lig., post. uterus, post. broad lig. Endometriosis can be induced in baboons by ligation of the cervix 27
28 : Coelomic metaplasia theory Metaplastic change in the coelomic epithelium (peritoneum and pleura): spontaneous or induced Supporting evidences: Endometriosis has been found in premenarcheal girls Pleural and pulmonary endometriosis Endometriosis in men treated with high doses of estrogen In vitro, ovarian surface epithelium can be induced by estradiol to form endometrial glands 28
29 : Metastasis theory Hematogenous or lymphatic spread Unusual sites of endometriosis: brain, colon A 35 year-old female complained of severe abdominal pain and constipation as well as bloody stool during menses. Colonoscopy showed a fungating mass, which turned out to be a endometriotic lesion. (BMJ,2003) 29
30 : The genetic basis Genetic predisposition: 6-9 times more prevalent among first-degree relatives of affected women than in the general population Oxford endometriosis gene study: Resistance to apoptosis: Bcl-2/bax family Attachment to peritoneum: integrins Invasion of peritoneum: MMP High estrogen environment that stimulates growth of endometriosis: aromatase, 17?HSD type 1/type 2 30
31 : The immunologic basis A wide range of immunologic abnormalities have been described in women of endometriosis The peritoneal fluid of affected women contains increased numbers of immune cells which promote the disease by secreting a variety of cytokines and growth factors that stimulate endometriotic attachment, invasion, proliferation, and neovascularization Women with endometriosis have high prevalence of auto immune diseases(.SLE,R.A) 31
32 : (Lancet, 2004, modified) Immunobiology of endometriosis 32
33 : Clinical Presentation Pelvic pain Chronic pelvic pain 70 % severe dysmenorrohoea 90% dyspareunia 75% Infertility 55% Abnormal Uterine Bleeding Pelvic mass (Endometrioma) 33
34 : Pelvic pain There is no relationship between stage, site, or morphological characteristics and the degree of pain Pelvic pain: diffuse, dull, and deep, may radiate to the back, may be associated with nausea, diarrhea and rectal pressure Dysmenorrhea: begins before menses and persists throughout menses Intermenstrual pain: 1/2 to 2/3 of patients Dyspareunia: disease involving the cul-de-sac and rectovaginal septum Associated activities: May include , dysuria, or dyschezia Other sites of pain : Muscle regions, Distant tissues 34
35 : Endometriosis Umbilicus & Surgical scars Cyclical pain & swelling Symptoms
36 : Mechanisms of pain (1) Actions of inflammatory cytokines in the peritoneal cavity: mild (early stage) disease or severe (advanced stage) disease (2) Direct and indirect effects of focal bleeding from endometriotic implants: mild disease or severe disease (3) Irritation and direct infiltration of nerves in the pelvic floor: severe disease Hormonal modulation: pain threshold and tolerance are lowest just prior to and during menses 36
37 : Infertility mechanisms 37
38 : signs asymptomatic Fixed retroverted uterus Tenderness in pod or in adnexa Fixed adnexal masse tenderness/nodularity nin u.s ligament Visible lesion in vagina or cervix. 38
39 : DIFFERENTIAL DIAGNOSIS 39 Ovarian cysts. 2. Pelvic inflammatory disease . 3. Other causes of nodularity in pouch of Douglas as tuberculous peritonitis and metastases of ovarian cancer. 4. Causes of haematuria , bleeding per rectum and acute abdominal pain if the patient is presented by one of these symptoms. 5. Asymmetrical enlarged uterus
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42 : Endometriosis / risk of cancer 42 Ovarian Clear cell & Endometrial cell carcinomas Breast cancer, Melanoma & NHL
43 : Diagnosis of endometriosis Clinical diagnosis: history and physical examination (rectovaginal septum lesion, fixed adnexal mass, tenderness/modularity of U-S lig.). ? poor predictive value CA125: not useful as screening test because it is elevated in deep infiltrated endometriosis and other diseases (elevated in menstruation, early pregnancy, PID, and myomas); low sensitivity; predicts the success of surgical but not medical treatment 43
44 : Endometriosis Investigations Laparoscopy ‘Gold standard’ diagnostic test for endometriosis It permits a “see & treat” approach, although its effectiveness may be limited by the nature of the disease and the surgeon's skill
45 : Endometriosis Ultrasound For Endometriomas sensitivity 83% & specificity 98% Confused with functional cysts
46 : Endometriosis CT scan Endometriomas may appear solid, cystic or mixed Because of poor specificity & high radiation, CT has been replaced by MRI
47 : Endometriosis MRI Role is limited in visualizing small endometriotic implants and adhesions More useful for lesions in extraperitoneal locations & the contents of pelvic mass More frequently used in staging & treatment response monitoring
48 : Appearance of endometriosis Peritoneal endometriosis Ovarian endometriomas Deep infiltrating lesion. Peritoneal endometriosis Brown or red implants Black (“Powderburn /gunshot”) serous or clear vesicles , polypoida (“Atypical or subtle lesion”) Deep infiltrating disease extends > 5mm beneth peritoneum morphologically like adenomyosis arising in mullerian rest in r.v septum ,u-s ligament,vagina ,bowel ,bladder and ureter Endometriosis May Be Associated with Peritoneal Windows 48
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53 : Classification SYSTEM/ Staging Revised AFS System or ASRM: Most Often Used Staging is designed to predict futur fertility There is no correlation b/w the staging and degree of the pain or prognosis of the treatment. Several Proposed Schemes Ranges from Stage I (Minimal) to Stage IV (Severe) Staging Involves Location and Depth of Disease, Extent of Adhesions 53
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55 : Stages of Endometriosis First stage: score is 1---5 minimal disease --small amount of brownish, reddish, blue-black, white, or clear implants Second stage:score 6-----15 moderate disease -- deeper and more numerous than stage one 55
56 : continue Third stage: score 16------40 moderate disease -- many deep implants, small endometriomas on ovaries and some filmy adhesions Fourth stage: score > 40 severe disease -- many deep implants and dense adhesions, large endometriomas on ovaries, rectum may adhere to the back of the uterus 56
57 : 57
59 : Endometriosis Treatment Consideration Age Symptoms Stage Infertility
60 : Treatment of endometriosis: Overall Approach Recognize Goals: – Pain Management – Preservation / Restoration of Fertility Discuss with Patient: – Disease may be Chronic and Not Curable – Optimal Treatment Unproven or Nonexistent 60
61 : Treatment of Endometriosis Management of pain Treatment of infertility 61
62 : Management of Pain Medical treatment Surgical treatment Combined surgical and medical treatment 62
63 : Treatment of Infertility Removal of disease Surgery improve conception rates at all stages Ovulation induction Gonadotropins with ovarian suppression Insemination with either clomiphene or FSH Medical suppression of ovarian function No benefit Assisted reproductive technology
64 : dietary changes some women have found relief by giving up caffeine, sugar, or alcoholic beverages incorporate more organic vegetables and fewer processed foods vitamins and herbs the B complex vitamins: improves emotional symptoms of endometriosis is linked to the breakdown of estrogen in the body vitamin E and selenium when taken together, these have been reported to decrease endometriosis-related inflammation Chinese herbal teas other people benefit from biofeedback, massage, acupuncture, Relaxation exercises, TENS Non HORMONAL treatment Medical treatment of pelvic pain
65 : cont Non- hormonal +Nsaids + opoids + TCA + SSRIs 65
66 : Hormonal treatment COC Progestogens LNG-IUS Gastrinon Danazole GnRH Analogue 66 Majority of therapies act by ovarian suppression & induction of amenorrhea. Symptoms recurs after cessation in a proportion of Rx may potentially be long term All therapies has similar efficacy but there tolerability in term of S/E & risk is important when selecting the most appropriate Rx.
67 : NSAIDS: NSAIDS: all significantly better than placebo, studies vary which one is best Naproxen >mefanemic acid>aspirin Naproxen=ibuprofen Naproxen only drug with significant SEs 67
68 : Endometriosis Hormonal Treatment Produces pseudo pregnancy or pseudo menopause Danazol Progestins Gestrinone Combined oestrogen-progestogen Pills GnRH agonists.
69 : Endometriosis Hormonal Treatment Indications Small & superficial lesions Recurrence after conservative surgery Preoperative for 6-12 wks to decrease size Postoperative for residual lesions When surgery is contraindicated or refused by the patient. Enometriosis in Rectovaginal septum & laparotomy scars doesn’t respond to Hormonal therapy
70 : Endometriosis Hormonal Treatment The choice between the COCPs, Progestogens, Danazol & GnRH agonists depends principally upon their side-effect profiles because they relieve pain associated with endometriosis equally well - Clinical Green Top Guidelines, 2000
71 : Progestogens May be as Effective as GnRH-a for Pain May be Taken Long-Term 6---9 months Relatively Inexpensive High doses oral progestin MPA (provera commonly used) 20-100 mg daily or norethindrone acetate (primolut-n) 40 mg daily, DP 150 mg Semi-Monthly Mechanisms: atrophy of endometrial tissue and inhibition of ovulation (higher doses) Side effects: breakthrough bleeding 33%(may be treated by conjugated estrogen 1.25 mg qd or estradiol 2 mg qd for a week), weight gain, fluid retention, breast tenderness, depression, and poor lipid profile , amenorrhea. 71
72 : Endometriosis Combined pills Well tolerated & can be continued for long term 1 pill/ day either continuously or cyclically Continuous regimen is superior in patients with dysmenorrhea Minimizes retrograde menstruation Choose ocp wth least estrogenic effect and high androgenic effect Mechanisms: atrophy of endometrial tissue, absence of retrograde menstruation (high estrogen and high progesterone state ? pseudopregnancy Adverse effects: weight gain, abnormal bleeding & HTN
73 : The first drug ever approved for the treatment of endometriosis in the U.S. 2. Orally administered isoxazol derivative of 17?-ethinyl testosterone 3. Mechanisms: inhibit steroidogenic enzymes and LH surge ? low estrogen and anovulation ? no retrograde menstruation free testosterone ? + low estrogen ? inhibit endometriotic growth. 4. Weak Androgen, Suppresses LH/FSH, Causes Endometrial Regression, Atrophy, 5. Doses: 600-800 mg daily( Expensive) 6. Side effects: weight gain, fluid retention, decreased breast size, acne, atrophic vaginitis, irreversible deepening voice, poor lipid profile danazol 73
74 : Endometriosis GnRH agonists ? FSH & LH & results in endometrial atrophy & amenorrhea Intranasally or SC or IM with a frequency of twice dly to once in 3 months up to 3 - 6 months Adverse effects: transient vaginal bleeding, hot flushes, vaginal dryness, ? libido, breast tenderness, insomnia, depression, irritability, fatigue, headache, osteoporosis, ? elasticity of skin GnRH agonists + Add-back therapy (estrogens & progestogen) – less side-effects but with same efficacy, can be continued beyond 6 months
75 : LNG releasing intrauterine system Limited data on the effectiveness of the LNG-IUS in the management of pain in endometriosis. No suppress of ovulation Acts locally on the endometrium. Reduction of menstrual pain is better with LNG-IUS then GnRH. 75
76 : Gossypol Is a phenolic compound extracted from the seed , stem and root of the cotton plant. It is a suppressor of FSH and LH , producing endometrial atrophy in about 50% of patients after 3 months . Dose : 20 mg daily for 2 months then 25 mg twice weekly for main­tenance . Side effects : include electrolyte disturbance especially hypokalaemia and alteration of hepatic and renal functions .
77 : Gestrinone Testosterone (Clin. Gynecol. Endocrinol. Infertil., 2005) Danazol A 19-nortestosterone derivative Has androgenic, antiprogestinic and antiestrogenic actions Doses: 2.5-10 mg body weight. Side effects: similar to danazol, but less pronounced gestrinone 77
78 : GnRH Analogs depletion of pituitary hormones which regulate the release of estrogen from the ovaries estrogen level decreases to menopause levels (reversible menopause) ovulation does not occur endometrium does not grow may reduce endo-related pain Intranasally or SC or IM with a frequency of twice dly to once in 3 months up to 3 - 6 months
79 : Endometriosis Adverse effects: transient vaginal bleeding, hot flushes, vaginal dryness, ? libido, breast tenderness, insomnia, depression, irritability, fatigue, headache, osteoporosis, ? elasticity of skin GnRH agonists + Add-back therapy (estrogens & progestogen) – less side-effects but with same efficacy, can be continued beyond 6 months Not used in pregnancy ,breast feeding and undiagnosed vaginal bleeding
80 : Gonadotophin-releasing hormone agonists for the treatment of endometriosis 80
81 : Aromatase In Endometriosis Aromatase is key for the biosynthesis of estrogen In patients aromatase expression is higher in endometriosis tissue than in normal endometrium In endometriosis tissue aromatase activity is stimulated by prostaglandin Estrogen synthesized by endometriotic tissue stimulates growth of lesions
82 : LIMITATIONS OF DRUG THERAPY / medical management Only shrinks some types of endometriosis which are estrogen sensitive i.e red and blister appearance not brown, black and white Shrinkage not complete- usually leaves micro disease Results for infertility treatment no better than no treatment Does not deal with adhesions 82
83 : Surgerical treatment of endometriosis ? Removal of Ovaries at Hysterectomy ? Need for Progestins if ERT Given ? Adjuvant Treatment Postoperatively ? Lupron Challenge Test for Diagnosis ? Is Endometriosis Best Treated Surgically, Medically or Both 83 Issues
84 : Endometriosis Surgical management Objectives: restore normal anatomy, excise or destroy all visible lesions as possible, prevent or delay recurrence. Operate in the follicular phase instead of in the luteal phase Conservative – Excision, Cauterization & Evaporation Surgeries for pain - Uterosacral Nerve Ablation (LUNA), Presacral Neurectomy Radical surgeries - Hysterectomy +/- BSO in women wth advance disease and completed faimly.low dose estrogen and progestogen given. postoperatively.estrogen only caused adenocarcinoma from residual endometriosis Surgeries for Endometrioma – Cystectomy, Drainage & coagulation, Fenestration
85 : Endometriosis Surgical management Laparotomy Vs Laparoscopy Efficacy is same Laparoscopy – less cost & shorter recovery time even in women with advanced endometriosis
86 : Endometriosis Laparoscopic management 1. Excision 2. Vaporization 3. Fulguration & Desiccation 4. Cystectomy for endomterioma 5. Drainage & Coagulation for endometrioma 6. Fenestration for endometrioma No RCTs available to compare these procedures Cystectomy offer better results than drainage & coagulation for Endometrioma If no cyst wall is present, Fenestration followed by GnRH agonists may prove beneficial
87 : (Surgical management of endometriosis, 2004) Ovarian endometrioma: excision is better than drainage and ablation as regards to recurrence and pregnancy rates. (Hum. Reprod., 2005)
88 : Dissection of an Endometrioma Tube Ovary Incision Removal Result
89 : (Surgical management of endometriosis, 2004) Excision of adhesion bands
90 : Removal of Endometriosis
91 : Surgery Presacral and uterosacral neurectomies where the nerves transporting sensation to the uterus are cut to lessen the pain Micro-laparoscopy surgical equipment less than 3mm in diameter it can be passed through a needle without making an incision minimal amount of local anesthesia Laparotomy more extensive procedure, full abdominal incision, longer recovery period (4-6 weeks) purpose: perform delicate microscopic surgery
92 : Surgery Hysterectomy used only as a last resort complete removal of the uterus and possibly some of the other reproductive organs does not guarantee relief from symptoms and pain endometriosis is one of two leading indicators for hysterectomy for women under the age of 54 (Perloe, 1995) if both ovaries are not removed, 30% or more women will experience recurrent endo symptoms (Perloe, 1996) eliminates pain in 90% of cases (Olive and Schwartz, 1993) following surgery, women usually take hormones to control the endometriosis and help keep it from growing back- hormones also help reduce the pain
93 : outcome was poorest in minimal endometriosis much better in moderate & severe cases - Sutton CJ et al, Fertil Steril 1994 Surgical management
94 : Endometriosis Combination of Hormonal & Surgical Postoperative Danazol & Medroxyprogesterone for 6 months lowered the pain scores significantly – Telimaa S et al, Gynecol Endo, 1987 Postoperative GnRH agonist for 6 months lowered the recurrence rates but with no change in pain scores – Parazzini F et al, AJOG, 1994 Sufficient data is not available to conclude that hormonal & surgical combination is associated with significant benefits. The possible benefits should be weighed in the context of the adverse effects & costs of these therapies - Cochrane review, May 2004
95 : TREATMENT OF INFERTILITY No role for medical therapy with hormonal drugs Laparoscopic ablation of minimal – mild endometriosis may improve fertility rates - Cochrane review, 2004
96 : Endometriosis IUI The presence of endometriosis does not generally impair the results of IUI Ovarian hyperstimulation using Gonadotrophins with IUI is better than no treatment or IUI alone Nulsen Jc et al, Obst Gyn, 1993 & Tummon IS et al, Fertil Steril, 1997
97 : Endometriosis & IVF The presence of endometriosis does not generally impair the results of IVF but it increases the risk of infection. It is preferable not to cauterize ovarian endometrioma if IVF or ICSI is indicated for fear of destruction of ovarian tissues.


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