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AUB.ppt
- 1.
- 2. DEFINITION : • Anyuterine bleeding outside the normal volume, duration, regularity or frequency.
- 3. NORMAL MENSTRUATION : •Cycle interval 28 days (21-35 days) • Menstrual flow 4 to 5 days • Menstrual blood loss 35ml (25 to 80ml)
- 4. MENORRHAGIA : • Cyclicalbleeding at normal intervals the bleeding is either excessive in amount (>80ml) or duration (>7 days) or both. • Menotaxis : prolonged bleeding
- 5. Polymenorrhoea (Epimenorrhoea) • Cyclicalbleeding where the cycle is reduced to less than 21 days and remains constant at that frequency. Polymenorrhagia (Epimenorrhagia) • When the frequent cycle is associated with excessive and or prolonged bleeding.
- 6. • METRORRHAGIA :Irregular, a cyclical bleeding from the uterus. • MENOMETRORRHAGIA : Bleeding is so irregular and excessive that the menses cannot be identified at all.
- 7. • Oligomenorrhoea :Menstrual bleeding occuring > than 35 days apart and which remains constant at that frequency. • Hypomenorrhoea : When the menstrual bleeding is unduly scanty and lasts for less than 2 days.
- 8. FIGO 2011 CLASSIFICATIONOF AUB – PALM COEIN Structural causes (PALM) • P - Polyp • A - Adenomyosis • L - Letomyoma • M - Malignancy
- 9. Nonstructural systemic causes(COEIN) • C - Coagulopathy • O - Ovulatory dysfunction • E - Endometrial • I - Iatrogenic • N - Not yet identified
- 10. Definition : • Abnormaluterine bleeding in the absence of organic pelvic pathology, systemic diseases, endocrine disorders, blood dyscrasias, iatrogenic causes and pregnancy. DUB : Dysfunctional uterine bleeding
- 11. • Therefore thediagnosis of DUB is based on exclusion of organic lesions. • DUB is due to dysfunction of hypothalamo- pituitary ovarian axis.
- 12. PATHOGENESIS OF DUB: • Endometrium normally produces, prostaglandin from arachidonic acid which is a fatty acid. • PGE2 and PGI4 are vasodilators and antiplatellet aggregates. • PGF2__ and thromboxane A 2 – vasoconstriction and platelet aggregates.
- 13. • Progesterone isresponsible for secretion of PGF2__ . • In onovulatory cycles, the absence of progesterone and therefore PGF2__ causes menorrhagia. • In some cases tissue plasminogen activator (TPA) which is a fibrinolytic enzyme is increased leading to menorrhagia.
- 14. Classification of DUB Anovulatory (80%) Ovulatory (20%) Thresholdbleeding of puberty menorrhagia Irregular ripening Metropathia haemorrhagia Irregular shedding Premenopausal DUB IUCD insertion Following sterilization operation
- 15. PUBERTY MENORRHAGIA : •DUB in the 1st year of menarche • Anovulatory cycles • Due to immaturity of the hypothalamopituitary ovarian axis. • Takes 18 months to 2 years for cycles to be regularised. • No dysmenorrhoea • Unopposed oestrogen causes endometrial hyperplasia.
- 16. RULE OUT : •Hypothyrodism • Bleeding disorders • Genital TB (early stages) • Liver disorders • Feminizing ovarian tumours granulosa cell and theca cell tumours.
- 17. INVESTIGATION : • Bloodgroup Rh, HB%, PCV, peripheral smear. • Platelet count • BT, CT, PT APTT • TFT • LFT • USG – PCOD to R/O organic pelvic patho condition of uterus – rarely fibroid. • Sarcoma Botyroides oestrogen producing ovarian tumours.
- 18. TREATMENT : • Assurance •Correct anaemia • NSAIDS – Mefenamic acid 500mg. TDS x 5 days IBUPROFEN 400mg. BD x 3 days. • Antifibrinohytic agents e.g. transexamic ACID 500mg. TDS x 5 days. • Ethamsylate 500mg TDS x 5 days to decrease the capillary fragility.
- 19. • Harmonal –in polymenorrhoea / polymenorrhagia start MPA (medroxy progesterone acetate) 10mg OD from D5 to D25 x 3 months. • In Menorrhagia – start MPA 10mg OD from D15 to D25 x 3 months. • OC pills to regularise the cycle for 3 months
- 20. D & Cnot done – only as a last resort. • 90% patients respond to this type of treatment without compromise on reproductive function. • Desmopressin – indicated in Von Wille brand’s disease and factor VIII deficiency. It is a synthetic analogue of arginine – vasopressin given IV or intranasal.
- 21. DUB in reproductiveage group and perimenopause: • Clinical features are similar. • No dysmenorrhoea as cycles are anovulatory. • R/O pregnancy in reproductive age group. • R/O malignancy in perimenopausal women with a fractional curettage.
- 22. Ovular DUB –20% IRREGULAR RIPENING IRREGULAR SHEDDING (Halban’s Disease) Due to corpus luteum insufficiency Due to persistence of corpus luteum Break through bleeding occurs before the actual menses in the form of spotting or brownish discharge. Menses comes on time but is prolonged not heavy. Progesterone given during the luteal phase (D15 to D25) cures the spotting. Progesterone can suppress the bleeding but needs to be taken on tapering dose for 20 days to complete the cycle.
- 23. Metropathia Haemorrahagia (Schroeder’sdisease) • Seen in women between 40 to 50 years. • Not related to parity. • Typical history – 6 to 8 weeks amenorrhoea followed by menorrhagia (painless). • Uterus is just bulky (myohyperplasia). • HPE – cystoglandular hyperplasia or Swiss cheese appearance. • May be associated with follicular cyst ovary (1 or both)
- 24. Investigation : • Bloodgroup Rh, HB% , PCV • Platelet count • PT, APTT, BT, CT • TFT • LFT
- 25. • USG – toR/O organic pelvic pathology – size of uterus, ET – Condition of ovaries • Hysteroscopy, SIS (Saline infusion sonography). • Fractional curettage – endometrial study to R/O malignancy - Endometrial CA
- 26. TREATMENT : • General– correct anaemia • NSAIDS – Mefenamic acid 500mg BDx 4 to 5 days • Antifibrimolcytic drugs – – Tranexamic acid 500mg TDS x 4 to 5 days – Capillary Haemostatic – Ethamsylate 250mg TDS x 4 to 5 days. – Ethamsylate can also be started 5 days prior as it decrease capillary fragility.
- 27. PROGESTERONE – tostop bleeding • MPA 10mg TDS x 5 days full by 10mg BD x 5 days full by 10mg HS x 10 days. • Withdrawal bleeding in 2 to 5 days blood loss WML. • Further course MPA 10mg HS x 20 days start from 5th to 25th day OR • Depot medroxy progesterone acetate. DMPA – 3 monthly infections decrease the no. of menses in a year.
- 28. Medical curettage : •To arrest bleeding in acute phase Northisterone acetate (Primolut N) 5mg TDS x 5 days 5mg BD x 5 days 5mg HS x 5 days
- 29. • ORMELOXIPHENE (SERMalso used as nonsteroidal OC pills – Saheli) in DUB – 60mg twice weekly for 12 weeks and thereafter weekly. • It does not cause breast and uterine CA because of its anti oestrogenic effect. • It also protects the bone and CVS.
- 30. • Mirena –IUCD. Avoids the side effects of oral harmones. • It directly suppresses endometrium with minimal side effects. It has no action on the ovaries, therefore E2 and progesterone level remain normal. • Decrease blood loss by 70 to 80% in 3 months. • Acts as a contraceptive.
- 31. MIRENA IUCD • 52mglevonorgestrel • Last for 5 years
- 32. Disadvantages of Nirema: • Slightly difficult to insert. • Takes 3 months to become effectie. • Amenorrhoea in 20 to 25 % which is not desirable in younger women. • Hysterectomy required in 25% by the end of 3 years because of recurrence of Menorrhagia.
- 33. MIS – MinimalInvasive Surgery : Role of D & C : • Diagnostic – – To note the type of endometrium. – To detect endometrial CA – To detect genital TB • Therapeutic – – 30 to 40% relieved of menorrhagia at least for a short period.
- 34. ABLATIVE THERAPY : 1stGENERATION • Hysteroscopic endometrial ablation by resectoscope, loop, rollerball coagulation and laser (TCRE – Transcervical endometrial resection) 2nd GENERATION • Radiofrequency induced thermal ablation cavaterm balloon therapy. • Microwave endometrial ablation (MEA) laser therapy.
- 37. HYSTERECTOMY FOR DUB: LAVH : Laparoscopy assisted vaginal hysterectomy. TLH : Total laparoscopic hysterectomy. VH : Vaginal hysterectomy. TAH : Total abdominal Hysterectomy. INDICATIONS : • If medical / MIS falls or DUB recurs • In women > 40 years who opt for hysterectomy as a primary treatment.
- 38. VAGINAL HYSTERECTOMY ISCONTRAINDICATED IF : • Uterus is grossly enlarged. • Previous surgery with possible adhesions, fixity and limitation of uterine mobility. • Presence of endometrioses or adnexal mass. • Women <50years ovaries to be conserved unless diseased.
- 39. ENDOMETRIAL HYPERPLASIA : •Anovulatory cycles with unopposed Estrogen activity on endometrium. • Metropathia haemorrhagica • Obese women • Polycystic ovarian disease • Woman on tamoxifen • Menopausal women on HRT without progesterone • Feminizing ovarian tumour.
- 40. TYPES OF ENDOMETRIALHYPERPLASIA : • Simple endometrial hyperplasia - without Atypia – 1% chance of malignancy - with atypia – 8% • Complex endometrial hyperplasia - Without atypia – 3% chance of malignancy - With atypia – 29%