Benign dis of upper g tract

Benign Diseases
of the Upper
Genital
Tract
Dr. Amira Badawy
Lecturer Ob/Gyn
Faculty of Medicine – Alexandria
University

1. A pregnant woman with fibroid uterus
develops acute pain in abdomen with low
grade fever & mild leucocytosis at 28
week. The most likely diagnosis is
a) Preterm labor
b) Torsion of fibroid
c) Red degeneration of fibroid
d) Infection in fibroid

1. A pregnant woman with fibroid uterus develops acute
pain in abdomen with low grade fever & mild leucocytosis
at 28 week. The most likely diagnosis is
a) Preterm labor
b) Torsion of fibroid
c) Red degeneration of fibroid
d) Infection in fibroid

2. Least common complication in fibroid is
a) Menstrual disorder
b) Malignancy
c) Urinary retention
d) Degeneration

3. Submucosal fibroid is diagnosed by all except
a) Hysteroscopy
b) Hysterosalpingography
c) Transabdominal USG
d) Laparoscopy

4. The drug which has no effect on the size of fibroids is
a) GnRH agonist
b) Danazol
c) Progesterone
d) Mifepristone

5. all of the following are indications for myomectomy
except
a) Associated infertility
b) Recurrent pregnancy loss
c) Pressure symptoms
d) Red degeneration

6. A 29 yr old nulliparous woman complains of severe
menorrhagia & lower abdominal pain since 3 months. On
examination there was a 14 weeks size uterus with fundal
fibroid. The treatment of choice is
a) Wait & watch
b) GnRH analogue
c) Myomectomy
d) Hysterectomy

7. pressure symptoms are usually seen in which type of
fibroid?
a) Submucous
b) Subserous
c) Intramural
d) All

8. Treatment of choice in a 42 yr old with bleeding P/V
due to multiple fibroids, up to 20 weeks size is
a) TAH with BSO
b) TAH
c) Myomectomy
d) Vaginal hystertectomy

8. Treatment of choice in a 42 yr old with bleeding P/V
due to multiple fibroids , up to 20 weeks size is
a) TAH with BSO
b) TAH
c) Myomectomy
d) Vaginal hystertectomy

9. Malignant prevalence in a fibroid is
a) 0.5%
b) 1%
c) 2%
d) 5%

10. Interstitial myomas predispose to menorrhagia by
a) Inhibiting uterine contractility
b) Degeneration
c) Erosion of endometrium
d) Cause not known

DEFENITION & INCIDENCE
“ LEIOMYOMATA, MYOMATA, FIBROIDS “
A solid benign tumours of the uterus.
Most common solid pelvic tumours.
Most common benign uterine tumours.
25-50% of women.
More at reproductive age group (35-45).
More in Nullipara, low parity, Blacks, Obese, non-smokers
Seen in up to 75% of hysterectomy specimens

AETIOLOGY
Unknown.
Persistent E2 stimulation (nullipara).
Hyper-E2 (reproductive age/never pre-pupertal nor post-menopausal/ass
with EQ & endom. hyperlpasia)
E2 receptors
Local E2 metabolism.
Racial & inherited factors

Mechanisms responsible for myoma growth

TYPES
 3 types or grades (0 / 1 / 2).
 causes symmetrical uterine enlargement.
 liable for ulceration & infection.
 act as FB  uterine contractions  cx dilatation 
expulsion.
 causes AUB even if small in size, & may  inter-menstrual
bleeding.

TYPES
 = mural fibroids.
 all fibroids start as ISF
 usually multiple.
 all are capsulated (pseudo-capsule).
 causes symmetrical uterine enlargement.

TYPES
 sessile or pedunculated (types 5,6,7).
 surrounded by serosa (partially or mostly).
 causes Asymmetrical uterine enlargement.
 may attain large size before causing symptoms which are
usually pressure symptoms.
 special types:
Intra-ligamentary.
Parasitic
Retro-peritoneal (intra-lig/pseudo-cx/behind UVP).

TYPES
1) True cx (intra-cx) fibroids (ant. / post. / lat./ central):
 more common at the post wall.
 causes cx elongation, stenosis & ballooning.
 may displace & compress UB & ureters.
 they are capsulated.
 causes pressure symptoms.
 if central  uterus is pushed up  “St. Paul’s lantern”

TYPES
2) Pseudo (false) cx fibroids:
 retro-peritoneal or inta-ligamentary, usually large.
 push the cx to one side but do not affect the cx canal.
 they are not capsulated.
 causes pressure symptoms.

TYPES
3) Sub-mucous cx fibroids:
 usually small.
 form cx polypi.
4) Cx fibroids from portio-vaginalis:
 usually small & sessile.
 may  polyp.

uterus
uterus
Cx
fibroid
Cx
fibroid
“St. Paul’s lantern”

Anterior (true) cx fibroid Central (true) cx fibroid

Posterior (false) cx fibroid Anterior (false) cx fibroid

PATHOLOGY - Gross appearance:
 Site: cx or corporeal (92%).
 Size: from microscopic to very huge size filling the abdominal cavity (up to 40 kg was
recorded)
 Shape: Spherical, flattened, or pointed according to the type.
 Count: single or multiple (92%).
 Consistency: firmer than the surrounding myometrium.
Soft fibroid occurs in pregnancy, cystic, vascular, inflammatory, & malignant
changes

PATHOLOGY - Gross appearance:
 Colour: pinkish white or greyish white
 Capsule: Pseudo-capsule [ compressed normal surrounding muscle fibers ],
Blood supply comes through it,
it is the plain of cleavage during myomectomy ,
its presence differentiate the myoma from adenomyosis,
all are capsulated except pedunculated SSF, pedunculated SMF, pseuodo cx fibroid.
 Cut section: whorly appearance, more pale than the surrounding uterine muscle,
 Blood supply: from the periphery, The tumor itself is relatively avascular.

PATHOLOGY - Microscopic appearance:
 Smooth muscle fibres + fibrous tissue

PATHOLOGY – pathologic effects:
 Endom.  thickened, congested, hyperplastric, increased surface area.
 Cavity  distorted & enlarged.
 Ut. position  pulled up, pushed laterally, prolapsed, RVF, inversion.
 Fallopian tubes  salpingitis (15%), stretched & elongated.
 Ovaries  CL haematoma.
 Anovulation.

PATHOLOGY – pathologic Varients:
 Intravenous leiomyomatosis.
 Leiomyomatosis peritonealis dissemination (LPD).
 Secondary changes.
 Leiomyosarcoma.

SECONDARY CHANGES
1) Degenerative Changes:
 Hyaline degeneration.
 Red degeneration (necrobiosis).
 Cystic degeneration.
 Fatty degeneration.
 Calcification.
 Necrosis.
 Atrophy.

SECONDARY CHANGES
“Hyaline degeneration”
 Commonest secondary change.
 Mainly involve the fibrous tissue component.
 More in SSF.
 Usually starts in the center of the fibroid.
 Cut surface = homogenous, pale, waxy, soft, with loss of whorly
appearance.
 Usually starts around menopause.

SECONDARY CHANGES
“Red degeneration”
 = Necrobiosis; as it shows dead parts (central) and living parts (peripheral).
 Exact aetiology is unknown.
 Common in pregnancy (2nd TM), due to:
• increased vascularity & venous stasis  the tumour enlarges with hemorrhage inside it.
• Thrombosis of the B.V.s of the capsule  ischaemia  incomplete necrosis  liberation
of toxins  haemolysis  red staining by blood piments.
 Mostly involve large fibroids.
 Cut surface = dark red colour +/- fishy odour).

SECONDARY CHANGES
“Red degeneration”
 Clinically = acute abdomen, the fibroid enlarges & becomes tender &
softer.
 Rx =
 Bed rest.
 Analgesics.
 Progesterones.
 +/- anti-pyretics & anti-biotics.
 Acute symptoms usually subsides gradually within 3-10 ds.

SECONDARY CHANGES
“Cystic degeneration”
1. True cystic changes :
 Rare.
 secondary to lymphangiectasia or EQ.
2. Pseudo-cystic changes :
 Secondary to red , hyaline or myxomatous degeneration (the tumour liquefies).
The affected tumour becomes soft in consistency.

SECONDARY CHANGES
“Fatty degeneration”
 Starts at the periphery of the fibroid, as lipids reach the fibroid through the
blood
 Fibroid become yellow & soft.
 Usually starts around menopause.
1. True Fatty degeneration :
 When fat droplets forms inside muscle fibres.
 Usually precedes calcification.
2. Fatty infiltration :
 Large fat droplets situated between muscle fibres.

SECONDARY CHANGES
“Calcificaion”
More common in old females.
Usually located at the periphery of the fibroid (as a shell)
The whole tumour may be calcified (Womb stone).
Fibroid become hard like bone.

SECONDARY CHANGES
“Necrosis”
 Total tissue death due to lack of blood supply.
 Usually starts at the center of the fibroid.
“Atrophy”
 Atrophy =shrinkage of the tumour.
 occurs due to estrogen withdrawal as after menopause, puerperium, or anti-estrogen use,
which  arrest of hormonal stimulation & reduced blood supply.
((All myomas decrease in size after the menopause except in calcification it remains
stationary, or with malignant change or HRT it increases in size))

SECONDARY CHANGES
2) Vascular Changes:
 Congestion.
 Oedema.
 Lymphangectasia
2) Infective Changes:

SECONDARY CHANGES
4) Malignant Changes: [< 0.5%]
 Leiomyosarcoma or fibrosarcoma.
 Suggestive findings:
a. Rapid increase in size.
b. PMUB.
c. Recurrence after removal.
d. Change in consistency.
e. Severe bleeding & severe pain.
f. Weight loss & cachexia.
g. Metastasis.

COMPLICATIONS
Torsion.
Haemorrhage.
Anaemia.
Secondary changes.
Incarceration in DP.
Ascites.
Infertility.
Abortion.
Other effects on pregnancy.

PRESENTATION
Asymptomatic:
 1/3 – 1/2 of cases.
 Accidentally discovered during examination.
 It is the commonest presentation, especially in SSF & ISF.

PRESENTATION
AUB: It is the commonest symptom, & fibroids are the commonest cause of AUB
 Menorrhagia or polymenorrhea: (commonest): This occurs due to:
 Associated hormonal imbalance (+/- anovulation) & endometrial hyperplasia.
 Surface ulceration of SMF.
 ISF acts as F.B. preventing full contraction of myometrium to decrease blood loss.
 Pelvic congestion.
 Increased uterine size, vascularity, & endometrial surface area +/- Adenomyosis.
 Metrorrhagia: due to:
 In SMF due to ulceration of the surface, necrosis of the tip, or secondary infection.
 Associated endometrial polyp.
 Anovulation & pelvic congestion.
 Associated malignancy (cancer body or sarcomatous change).
 Contact bleeding (post-coital): (rare)
 ulcerated or infected tip of submucous fibroid polyp.
 Post-menopausal bleeding: (rare)
 May be due to sarcomatous change or associated endometrial carcinoma.

PRESENTATION
Iron deficiency anemia.
Discharge:
 Leucorrhea & mucoid discharge due to pelvic congestion & endometrial hyperplasia.
 Muco-sanguinous discharge with ulcerated fibroid polyp.
 Muco-purulent discharge due to secondary infection (esp with SMF).
 Spontaneous & repeated abortion: more with SMF , due to:
 Endometrial congestion & hyperplasia.
 Cx dilatation.
 Encroachment upon the uterine cavity.
 Associated RVF & ovarian pathology.

PRESENTATION
 Pressure (bulk) symptoms
o Cervical fibroid:
 Anteriorly on the urethra causing acute retention of urine, or the bladder causing frequency of
micturition.
 Laterally on the ureters causing colic & back pressure on the kidneys.
 Posteriorly on the rectum causing dyschasia, constipation, & sense of incomplete defecation.
 Huge fibroid:
 On the pelvic veins causing edema, pain, & varicose veins in the lower limbs.
 On the GIT causing distension & dyspepsia.
 On the diaphragm causing dyspnea.
Swelling (mass):
 Either abdominal swelling due to large fibroid or vaginal swelling due to a polyp.

PRESENTATION
 Pain: uncommon
 Intermittent colicky pain in SMF (acts as F.B. in the uterine cavity).
 Pelvic heaviness & dragging pain (due to weight of large fibroids).
 Dull-aching pain & congestive dysmenorrhea due to pelvic congestion.
 Impaction in DP.
 Acute abdomen in red degeneration, torsion, ruptured vessel, inflammation, infection
& malignancy.
 Other associated causes: salpingitis, endometritis, or ovarian pathology.

PRESENTATION
Infertility[in 5-10% of cases]:
 Most important is the underlying predisposing factor as anovulation & hormonal
disturbance.
 Broad ligament fibroid may stretch or distort the tubes.
 Corneal fibroids may obstruct the uterine end of the tube.
 Reversed polarity of tubal peristalsis.
 Uterine irritability & contractions may interfere with implantation.
 SMF acts as F.B. interfering with proper implantation.
 Discharge from SMF may have a spermicidal effect.
 Cervical fibroid may obstruct or narrow the cervical canal.
 Associated endometriosis, salpingitis, or endometrial hyperplasia.
 Dysparunia.

SIGNS
 General examination:
 signs of chronic anemia.
 L.L. oedema & V.V.
 Abdominal examination:
 large pelvi-abdominal swelling in moderate & huge fibroids
(firm/mobile/not tender/dull/+/- ut. Soffle).
 Pelvic examination:
 symmetrically or asymmetrically enlarged uterus.
 Speculum examination
 fibroid polyp.

SIGNS
Pelvic examination:
1) Inspection & Speculum examination:
** Polyp. ** Dilated cx canal. ** Displaced cx. ** Bleeding & discharge.
2) Bimanual examination:
 Ballooned (enlarged) cx (=true cx fibroid)
 Mass felt through a vaginal fornix (pseudo-cx or intra- ligamentry)
 Cx felt continuous with the abdominal mass.
 Symmetrically or asymmetrically enlarged uterus.
3) Sounding:
 Elongated cx canal (true cx fibroid).
 Mal-directed cx canal (pseudo cx fibroid).
 Enlarged uterine cavity (ISF).
 To D.D. the origin of a polyp.

EFFECTS OF FIBROIDS ON PREGNANCY, LABOUR&
PUERPERIUM
 Pregnancy : Abortion
Pressure symptoms
Mal-presentation
Retro-displacement of uterus
 Labour : Preterm labour Uterine inertia
Dystocia 1ry PPH
 Puerperium: Subinvolution
Sec. PPH
Puerperal sepsis
Inversion

EFFECTS OF PREGNANCY ON FIBROIDS
 Increase in size & softening.
 Red degeneration.
 Impaction in pelvis.
 Torsion.
 Infection.
 Injury or Pressure necrosis during delivery.
 Rupture of sub-serous vein  Internal haemorrhage.

DIFFERENTIAL DIAGNOSIS
Causes of symmetrically enlarged uterus:
Pregnancy
Sub-involution of the uterus.
SMFs or ISFs.
Metropathia hemorrhagica.
Adenomyosis uteri.
Carcinoma or sarcoma of the uterus.
Pyo, hemato, or physometra.

DIFFERENTIAL DIAGNOSIS
Causes of asymmetrically enlarged uterus:
SSF.
Localized adenomyosis.
Ovarian, tubal, or broad ligament swelling.
Pregnancy in a rudimentary horn.

LABORATORY INVESTIGATIONS
 Pregnancy Test
 CBC.
 Coagulation Profile.
 Hormonal Assay (TFT, PRL)
 Blood Sugar Profile.
 Renal Function Tests.
 Liver Function Tests.

IMAGING + ENDOSCOPY
 TAS + TVS (2D/ 3D / Doppler).
 SIS.
 Plain X-Ray.
 HSG.
 IVU.
 CT.
 MRI.
 Laparoscopy.
 Hysteroscopy.

U/S has a sensitivity of 60%, a specificity of 99%, and an accuracy of
87%.
Uterine fibroids appear as concentric, solid, hypoechoic masses.
They may vary in the degree of echogenicity; (hypoechoic,
heterogeneous or hyperechoic), depending on the amount of
fibrous tissue &/or calcification.
Fibroids may have anechoic components resulting from necrosis.
Calcifications are hyperechoic, with sharp acoustic shadowing.

Endometrial stripe may be displaced by SMF(s).
Diffuse leiomyomatosis appears as an enlarged uterus with
abnormal echogenicity.
If fibroids are small & isoechoic, the only u/s sign = bulge in the
uterine contour.
Fibroids in the LUS obstruct the uterine canal  intr-ut. fluid
collection.

ECHOTEXTURE
Hypoechoic Shadowing 2ndry to whorls of fibrous tissue & edge artefacts
Echogenic
Isoechoic
Cystic areas Secondary to degeneration
Calcifications
Rim calcification
Clumps of calcification
LOCATION
Sub-mucosal
Associated with menometrorrhagia
Distort endometrial myometrial margins
Intra-mural Most common
Sub-serosal Distort outer uterine margins
Pedunculated
± Stalk
May present as adnexal mass
Cervical
At the anatomical site of the cervix
Hypoechoic and typically well defined
Broad ligament Simulate adnexal mass

MRI has a sensitivity of 86-92%, a specificity of 100%, and an accuracy
of 97% in the evaluation of fibroids (most accurate).
Fibroids appear as sharply marginated areas of low to intermediate
signal intensity on T1- & T2-weighted MRI scans (fibroid mapping).
An in-homogeneous area of high signal intensity may result from
haemorrhage, hyaline degeneration, oedema, or highly cellular fibroids.
MRI with IV gadolinium-based contrast material is not usually required
(to D.D. from adenomyosis).
Fibroid enhancement can be hypointense (65%), isointense (23%), or
hyperintense (12%) in relation to that of the myometrium.

MANAGEMENT
No treatment.
Medical.
Minimally invasive procedures.
Surgery.

NO TREATMENT
Indications :
• asymptomatic incidental fibroids
• Size < 12 weeks
• Fibroid in pregnancy or puerperium & nearing menopause
 Prerequisites:
 - Regular follow up every 6 months
 - Routine pelvic examination
 - Baseline imaging to compare the size.

MEDICAL MANAGEMENT
Up till now, no medication is approved for long-term administration.
Therefore, surgery remains the treatment standard for large symptomatic
myomata
So, medications are NOT a definitive treatment.
Indications:
Pre-operative till the time of surgery to correct general condition or to
reduce size of the fibroid.
Patient near the menopause, or newly married with minimal symptoms.
Red degeneration with pregnancy.
For symptomatic relief from pain.
To decrease menstrual blood loss.

MEDICAL MANAGEMENT
Symptomatic Rx:
Haematenics,
Haemostatics,
NSAIDs (anti-PG),
Anti-spasmodics,
COCs.

MEDICAL MANAGEMENT
Therapeutic Drugs :
 GnRH analogues.
 Progestogens : Oral/ IUCD.
 Aromatase inhibitors.
 Antiprogestogens (Mifepristone).
 SERMS & SPRM.
 Androgens ( Danazol, Gestrinone).
 Tamoxifen.

GnRH-Analogue:
 Triptorelin (Decapeptyl) 3.75 mg SC once a month X 3 months
 Leuprolide depot 3.75 mg SC once a month X 3 months
 Goseraline (Zoladex) 3.6 mg SC once a month X 3 months
 GnRH Antagonist:
Cetrorelix : 60 mg SC, repeated after 3-4 months if necessary.
Advantage --> NO initial flare up.
Disadvantages --> more expensive & requires daily intake.
GnRH analogue

 Advantages :
 Decrease in myoma size of by 20 - 50 %
 Decrease bleeding  increases Hb level
 Decreases blood loss during surgery
 Helps to convert hysterectomy into myomectomy
 Helps to converts abd. hysterectomy into vaginal hysterectomy
 Disadvantages :
 High cost.
 Hypoestrogenic side effects (artificial medical menopause).
 Effect is reversible (rebound increase in size after cessation).
 Rarely  ↑↑ bleeding due to degeneration.
 Occasionally difficulty in enucleation during myomectomy.
 may increase the risk of persistent myomata, as small ones would shrink in size &
would not be palpable during myomectomy
 Cannot be used before UAE.
GnRH analogue

Medroxy progesterone acetate (MPA)
Norethisterone acetate
From day 5 of menses, 1 x 2-3 x 21, 3-6 cycles.
Indication: To delay surgery
PROGESTERONE

For fibroid uterus <12 weeks size with menorrhagia.
 Contains 60 mg LNG (releasing 20 ug /day).
 Expulsion rates higher in presence of fibroids.
 Fibroids decreases in size after 6 - 12 months of use.
 May have variable effects on uterine myomata (depending
upon balance of growth factors).
LNG-IUS

 Directly inhibit estrogen synthesis & rapidly produce
hypoestrogenic state.
 Fadrozole/ Letrozole are used.
 71 % reduction occurred in 8 weeks.
 Appears to be promising therapy.
AROMATASE INH.

It is a PRM = RU486
 5 – 10 mg is tried
 Promising results
 Decrease in myoma volume by 26-74 %.
 No effect on bone mineral density
 Endometrial hyperplasia may limit its long term use.
Indication: To delay surgery
MIFEPRISTONE

 Selective Estrogen Receptor Modulator.
 60 mg /day, for 6 to 12 mths
 Higher doses ( 180 mg) are required for effective decrease
in size.
 Better if combined with GnRH-a
SERM (Raloxifen)

 5 - 25 mg/day.
 Mechanism of action is not known.
 Possible risk of endometrial hyperplasia is not studied.
SPRM (Asoprisnil)

MINIMALLY INVASIVE MANAGEMENT
MYOLYSIS
□ Laser Myolysis with Nd:YAG laser
□ Myolysis with bipolar needle
□ Myolysis with diathermy
□ Cryotherapy
□ Radiofrequency ablation.
□ HIFU
UTERINE ARTERY OCCLUSION
UAE
LUAO
Transient UAO

UTERINE ARTERY OCCLUSION
Mechanism of action
After uterine artery occlusion, the myometrium becomes hypoxic.
Within hours to days, clots become lysed within the myometrium
& collateral arteries begin to re-perfuse the uterus.
Myomata, in contrast, cannot lyse the clotted blood & re-perfuse.
They eventually become infarcted & die.
Clots form more quickly in myomata than in the myometrium.

UTERINE ARTERY EMBOLIZATION (UAE)
 By interventional radiologist, no pre-medication by GnRH-a.
 A catheter is passed retrograde through Right femoral artery to
bifurcation of aorta & then negotiated down to the opposite
uterine artery first.
 UAE  60 – 65 % reduction in size of fibroid.
 UAE  80 – 90 % improvement in menorrhagia & pressure
symptoms.
 High vascularity & solitary fibroid are associated with greater
chance of long term success.

UTERINE ARTERY EMBOLIZATION (UAE)
 Absolute contraindications = Pregnancy, active infection, desire for
fertility & suspicion of malignancy.
 Risk of ovarian failure must be counselled with patient.
 Embolic materials:
a) Typical or non-spherical polyvinyl alcohol (PVA) particles “Contour” = [500-
700 um]
b) Calibrated tris-acryl gelatin microspheres (TAGMs; Embosphere).
c) Spherical PVA particles (Contour SE)
d) Gelatin sponge particles -cut from gelatin sponge sheets- (Spongel). not yet
approved by the FDA.

Uterine Artery Embolization (UAE)

LAPAROSCOPIC UTERINE ARTERY OCCLUSION (LUAO)
Techniques of LUAO:
1. Vascular clips "endoclips" or "haemo-clips; two or three successive
preloaded 5-mm or 10-mm vascular clips are applied at the artery.
2. Laparoscopic bipolar coagulation of the uterine vessels (LBCUV).
3. Suture ligation & transaction of the vessels.
4. Ultrasonic coagulation of the uterine artery, & cut using UltraCision

( LUAO )
1) Site of incision at the pelvic
sidewall triangle.
2) The broad ligament is opened.

( LUAO )
3) The infundibulo-pelvic ligament is pulled
medially to expose the ureter at the pelvic
brim.
the extra-peritoneal portion of the
obliterated hypogastric artery is identified.
4) The lateral para-vesical space is opened

( LUAO )
5) The medial para-vesical space is opened.
6) The para-rectal space is opened

TRANSIENT UTERINE ARTERY OCCLUSION
Studies showed that only < 6 hours of occlusion are sufficient to
initiate fibroid death.
Due to ease of identification of uterine arteries transvaginally
access to & occlusion of uterine arteries with a Doppler-guided
device might offer an alternative to invasive procedures intended
to occlude uterine artery blood flow
The “flostat clamp” is a transvaginal vascular clamp & not a tissue
crushing clamp. When closed, the flostat clamp folds the vaginal
tissue & the uterine arteries against the lateral walls of the
uterus.

TRANSIENT UTERINE ARTERY OCCLUSION
The flostat clamp

MYOLYSIS
 It = in situ destruction of the tumour.
 Different methods for myolysis:
1. Laser myolysis : By ND:YAG laser.
2. Myolysis with bipolar.
3. Myolysis with diathermy.
4. Cryo-myolysis.
5. Radiofrequency ablation.
6. HIFU (high intensity focused ultrasound).
 Applicable if myoma 3 -10 cm size & < 4 in number

SURGICAL MANAGEMENT
 Indications:
• Symptomatic cases or uterus larger than 12 weeks size.
• Suspected malignancy (rapidly enlarging or post-menopausal
growth).
• Multiple huge fibroids liable to complications.
• Infertility.

SURGICAL MANAGEMENT
 Myomectomy :
 Laparotomy or mini-laparotomy.
 Vaginal.
 Laparoscopic.
 Lapaproscopic assisted minilaparotomy.
 Hysteroscopic.
 Hysterectomy.

 Indicated for females who want to preserve uterus for fertility or
for psycho-social reasons.
 Disadvantages :
 Much blood loss (compared to hysterectomy).
 +/- more operative time (compared to hysterectomy).
 Liability for recurrence (compared to hysterectomy).
 +/- uterine scar & future indication for CS (compared to minimally invasive Rx).
 Possibility of post-operative adhesions which may interfere with
future fertility (compared to minimally invasive Rx).
Myomectomy

Pre-operative preparations:
 Consent for possible hysterectomy (if needed)
 Preparation of blood or packed RBCs (for possible transfusion).
 Pre-operative measures to reduce operative blood loss
 Correction of anaemia.
Myomectomy

Techniques to reduce intra-operative blood loss:
1. Pre-operative:
GnRH-a (or other similar medical Rx)1-3 months prior surgery, to
reduce size & vascularity of myomata (but may increase difficulty of
operation).
Timing of operation is post-menstrual (minimal pelvic congestion)
Misoprostol (400 mcg, vaginal), 1 hours prior surgery.
Myomectomy

2. Intra-operative:
 Avoid anesthetic agents that induce uterine relaxation (e.g. halothane).
 Controlled hypotensive anaesthesia.
 Occlude uterine vessels by Bonney’s myomectomy clamp, rubber
tourniquet, sutures or UAE (or internal iliac artery ligation).
 Use Ring forceps to occlude the ovarian vessels.
 Ergometrine 0.25 mg IV (on opening the abdomen).
 +/- tranexaemic acid.
Myomectomy

2. Intra-operative (cont.):
 Inject Vasopressin (Pitressin) 10-20 IU in 100 ml normal saline, or
Epinephrine in the myoma-myometrial junction.
 Vertical midline incision of the uterus is the least vascular.
 Enucleate myomata through the proper line of separation from their
capsules.
 Remove all myomata through the least no. & smallest possible incisions.
 Obliterate tumour cavities & died spaces.
Myomectomy

Vasopressin (& other vasoconstrictors)
Intra-myometrial inj . of vasopressin into the planned uterine incision site for
each fibroid reduces blood loss.
Vasopressin acts by constricting the smooth muscle in the walls of capillaries,
small arterioles, & venules.
Use of Vasopressin may  (rare cases) of bradycardia, cardiovascular collapse,
& death.
C.I. of Vasopressin are some medical comorbidities (cardiovascular, vascular, or
renal disease).
This use of Vasopressin has not been approved by the US FDA.
Avoid intravascular injection (However, complications may result without IV
injection).

The maximal safe dose of vasopressin is not well established. A dilute
solution may  limit the total dose, as 20 units of vasopressin in 100 ml
saline.
The half-life of IM vasopressin is 10 - 20 minutes & the duration of action is 2
- 8 hours.
Epinephrine
A vasoconstrictor that is effective in reducing blood loss during myomectomy.
A randomized trial found that intra-myometrial injection of Bupivacaine (50
mL bupivacaine hydrochloride 0.25 percent) + Epinephrine (0.5 mL epinephrine
1 mg/ml)  ↓ ↓ blood loss compared with saline.
Intravascular injection of epinephrine may  acute cardiovascular adverse
events, (as vasopressin).

Tourniquet
 Procedure to apply a tourniquet:
 Palpate the broad ligament just above the level of the internal cervical os to identify a space that is free of
vessels & the ureter.
 Make a 1 cm incision (window) in this clear space bilaterally.
 Pass the tourniquet (or Foly’s cath) through the openings with the ends protruding anteriorly (to encircle
the isthmus).
 Pull the tourniquet tight & secure by a Kelley clamp. Take care to avoid enlarging the broad ligament
incisions or damaging surrounding structures.
 Use of number (1) suture as a uterine artery tourniquet during laparoscopic myomectomy has
been reported. In general, it is difficult to secure a tourniquet using laparoscopic instruments.
Occlusion of the ovarian arteries
 By placing a tourniquet or atraumatic vascular clamp (eg, bulldog clamp or Ring forceps)
bilaterally across the infundibulo-pelvic ligaments.
 Avoid lacerating the ovarian vessels or compressing the ureter.
 It is better to releas the tourniquet every 20 minutes, but outcomes for this practice have not
been evaluated

Techniques to reduce post-operative adhesions:
Use best operative approach to reduce adhesions (i.e. vaginal myomectomy,
hysteroscope, laparoscope, ..)
Reduce bleeding & avoid accumulation of intra-peritoneal blood.
Avoid rough manipulation & placing of inta-peritoneal towels to avoid serosal
injury.
Reduce no. of uterine incisions (as possible)
Bonney’s hood incision (for posterior wall myomata) + keep AVF uterus.
Buried sutures (as Baseball sutures).
Use absorbable sutures.
Peritoneal wash +/- Dextran solution, Ringer lactate solution or
dexamethazone.
Adhesion preventive substances.
Avoid infection (AB, Aseptic techniques, less bleeding, less operative time)
Myomectomy

Barriers for Adhesion Prevention:
1. Absorbable barrier “Intercede”:
 A mesh of oxidized regenerated cellulose.
 Placed on the suture line.
2. Non-aborbable barrier “GoreTex”, PTFE:
 Poly-Tetra-Flouro-Ethylene surgical membrane.
 May be sutured over uterine incisions.
3. Suprafilm (HAL-F)
 Bioresorbable membrane (Sodium Hyaluronate & Carboxy-methyl-cellulose).
4. Spray gel
  65% reduction in adhesions.
Myomectomy

Other considerations :
Preliminary diagnostic curettage to exclude endometrial carcinoma.
Try to keep the uterus AVF by: ventri-suspension, or plication of the
round ligaments & uterosacral ligaments.
Try to avoid opening of the uterine cavity, however, cavity is opened, it
should be carefully closed.
Care is to be taken not to compromise or injure the Fallopian tubes.
Myomectomy

Secondary
Incision
Excess
Tissue
Removal

•Vicryle
•4-0 or 5-0
•Small needle
•Running baseball
•Contineous
•Interrupted figure of 8
•Buried ends (knots).
Serosal Closure

Cervical Myomectomy:
Different according to the type & location:
1) Anterior  easy enucleated, transverse incision is made in UVP to push
the UB.
2) Posterior  more inaccessible, midline vertical incision to be away from
ureters & vessels, bed is difficult to reach.
3) Central  after enucleation  leaves elongated supra-vaginal posterior.

HYSTERECTOMY
Either abdominal or vaginal.
Indications:
 Patient > 40 years & completed her family.
 The number or site contraindicate myomectomy.
 Severe bleeding during myomectomy.
 Major damage of the uterus by myomectomy which affects
its function for pregnancy.
 Recurrent fibroids.
 Fibroids suspicious of malignancy.

HYSTERECTOMY
 Factors favouring vaginal hysterectomy:
 Uterus < 16 wks, preferably < 14 wks.
 No associated pathology like endometriosis , PID, adhesions.
 Uterus mobile & adequate lateral space in pelvis.
 Experienced vaginal surgeon.

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