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GY3Gynaecology Toronto Notes 2023

cardinal ligaments: extend from lateral pelvic walls and insert into lateral cervix and vagina

function:mechanical support, prevent prolapse

• broad ligaments: pass from lateral pelvic wall to sides of uterus; contain fallopian tube, round

ligament, ovarian ligament, nerves, vessels, and lymphatics. Within the broad ligament, the

uterine artery anastomoses with the ovarian artery

• infundibulopelvic ligament (suspensory'ligament of the ovary'):continuous tissue that connects ovary

to pelvic wall

• contains the ovarian artery, ovarian vein, ovarian plexus, and lymphatic vessels

• position of the uterus

anteverted (majority), retroverted, neutral

anteflexed (more common), retroflexed

.Round ligament

spensory

ligament olovary

undibulopelvic

ligament!

Posterior viow

Broad ligament

1. Anteverted anteflexed

2. Retroverted retroflexed

3. Retroverted anteflexed

©Kateryna Procunier 2016 after Marina Chang 2013

Cardinal ligam

Anterior viow Uterosacral ligament © Desmond Ballance 2006

Figure 2. Genital organs and positioning of the uterus

D. Fallopian Tubes

•8-14 cm muscular tubes extending laterally from the uterus to the ovary

•interstitial, isthmic, ampullary, and infundibular segments; terminates at fimbriae

•mesosalpinx: peritoneal fold that attaches fallopian tube to broad ligament

•blood supply: uterine and ovarian arteries

Determination of Uterine Position by

Clinical Exam

• If cervix faces anteriorly (under the

urethra and less easily accessible).

i.e.toward vaginal orifice,more likely

RETROVERTED UTERUS

• If cervix faces posteriorly (easily

accessible),i.e.toward sacrum or

tectum,more likely ANTEVERTED

UTERUS

• If uterus palpable on bimanual exam,

more likely ANTEVERTED UTERUS

• If uterus palpable behind the cervix

in the posterior fornix,more likely

RETROVERTED UTERUS

E. Ovaries

•consist of cortex with ova and medulla with blood supply

•supported by infundibulopelvic ligament (suspensory ligament of ovary)

•mesovarium:peritoneal fold that attaches ovary to broad ligament

•blood supply: ovarian arteries (branches off of aorta), left ovarian vein (drainsinto left renal vein),

right ovarian vein (drains into inferior vena cava )

"Water Under the Bridge”

The ureters run posterior to the uterine

arteries

Abdominal aorta

Ureter

Ovarian artery

Internal iliac artery Common Anatomy Questions in the OR

External iliac aitery What is the origin of the left and right

ovarian arteries

Descending aorta

What are the drainage sites for the left

and right ovarian veins?

Left to left renal vein,right to inferior

vena cava

What is the most common place to

locate the ureter?

In the pelvic brim,the ureter passes over

the iliac vessels.The ureter can also be

found near the medial leaf of the broad

ligament where the ureter runs under

the uterine artery

Which artery runs under the round

ligament?

Sampson's artery

Ovarian and tubal branches

of uterine artery

Sampson’s arteryIwilhin

round ligament)

Uterine aitery

Vaginal artery

=

S3

£ ri

£ L J

§

2

External pudendal aitery 0

Figure 3.Vascular supply +

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GY‘1Gynaecology Toronto Notes 2023

Menstruation

Menstrual Cycle

Day1D9y 5DayMDsy28Dayt

/ ; \—m

'

\ FSH

Progestsrone .

/ /

»

"

1

'

vV* V

Estrogen

i \ ,

I .- - -

§ - -

Degen«atirg , Prrnarytosde

Oeve'oping

co-pjsIjteun

r

i

FOUICULAR PRQLIFERATtVE PHASE (Variable Dnratiol) LUTEALSECRETORy PHASE (Fixed Duration - 14 days)

Early Mid late OVULATION Early-Mid tale

AEsritiPtliomendc:

preiions cycle)

TFSH acts cnoiarian grar Jesa Eravirgra’icias cord-iualo

seosieE

S:ditenswitchfremregaSi«ltipoatrie Snirtiackttregaiiileedbadt Hoienited oocyte

fettacklEariJPoiMTfSHSLM

InitiatingExacts

S

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TFSH

TLHpulsefreqoanty

TElrontolc«( espeoally !P senodaryto degeneration olcotpu tijn

trcndorwatolide

E peaks -> lHiiirge -

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eolation TPtromcorpusliltum

PJegalnt teedback E -•iFSH.iIH Poii!vel*

edPa«k:EandP -> TfSH.TlH S«gaivefeedback P -* FeediaekosHPOAns iFSH,iLH

TFSH -•tctliculaagrowth n TtolicultorgrowthIbyred^

:rg Oo-ra'tloi

'

depetsiKs. femainder

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Oranes •36halter LH surgye.dotnrantlolfel CesM'kvo olP frem corpuskattum

leases oocyte, ccrpusbtiumirtmnant *

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-ket1-2c0Tess FiOsrs 23KandSorya A-rn 2X3

PROGESTERONE

PROGESTERONE is the main hormone in the luteal

'

secretory

phase and is stimulated by LH.Increased progesterone

acts negatively on LH and is secreted by the corpus luteum

(remnant of dominant follicle)

ESTROGEN

ESTROGEN is the main hormone in the follicular/

proliferative phase and is stimulated by FSH.As the

level increases it acts negatively on FSH. The majority

of estrogen is secreted by the dominant follicle

CHARACTERISTICS

• Menarche10-15 yr

• Average 12.2 yr

• Entire cycle 28 ± 7 d with bleeding for 1-6 d

• 25-80 mL blood loss per cycle

Progesterone effects

• On the endometrium:cessation of mitoses (stops

building endometrium up),"organization" of glands

(initiates secretions from glands). (

Inhibits macrophages.

intcrlcukin-8. and enzymes from degrading endometrium

• On all target tissues: decrease estrogen receptors (the

"anti-estrogen" effect),decrease progesterone receptors

Estrogen effects

• On the follicles in the ovaries:reduces atresia

• On the endometrium: proliferation of glandular

and stromal tissue

• On all target tissues:decreases estrogen

receptors

Figure 4. Events of the normal menstrual cycle

E = estrogen; FSH = follicle-stimulating hormone; GnRH = gonadotropin-releasing hormone;HPO = hypothalamic-pituitary-ovarian;LH = luteinizing

hormone;P= progesterone

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Stages of Puberty <§

Stages of Puberty

• see Paediatrics. P36

• adrenarche: increased secretion of adrenal androgens; usually precedes gonadarche by 2 yr

• gonadarche: increased secretion of gonadal sex steroids;

-age 8 yr

• thelarche:breast development

• pubarche:pubic and axillary hair development

• menarche: onset of menses, usually following peak height velocity and/or 2 yr following breast

budding

“Boobs. Pubes.Grow. Flow”

Thelarche. Pubarche. Growth spurt,

Menarche

Tanner Stage

Premenstrual Syndrome Thelarche

1. None

2. Breast bud

3. Further enlargement of areolae and

breasts with no separation of contours

4.2° mound of areolae and papilla

5.Areolae recessed to general contour

of breast

• physiological and emotional disturbances that occur I -2 wk prior to menses and last until a few days

after onset of menses; common symptoms include depression, irritability, tearfulness, and mood swings

• synonyms:

“ovarian cycle syndrome," “menstrual molimina" (moodiness)

Etiology

• multifactorial: not completely understood; genetics likely play a role

• CNS-mediated neurotransmitter (serotonin, dopamine, GABA) interactions with sex steroids

(progesterone, estrogen, and testosterone)

• serotonergic dysregulation - currently most plausible theory'

Pubarche

1. None

2.Downy hair along labia only

3. Darker/coarse hair extends over pubis

4. Adult

-type hair with no thigh

involvement

5. Adult hair in distribution and type;

extends over thighs. Not all patients

achieve Tanner Stage 5. For image

see Paediatrics. P37

Diagnostic Criteria for Premenstrual Syndrome

• at least one affective and one somatic symptom during the 5 d before menses in each of the three prior

menstrual cycles

affective: depression, angry outbursts, irritability, anxiety, confusion,social withdrawal

• somatic: breast tenderness or swelling, abdominal bloating, headache,swelling of extremities,

joint or muscle pain, weight gain,fatigue

• symptoms relieved within 4 d of onset of menses and do not recur until at least day 13 of cycle

• symptoms present in the absence of any pharmacologic therapy, hormone ingestion, drug, or alcohol

use

• symptoms occur reproducibly during 2 cycles of prospective recording

• patient suffers from identifiable dysfunction in social or occupational performance

• consider a PRISM (Prospective Record of the Impact and Severity of Menstrual symptoms) calendar to

monitorsymptoms and confirm diagnosis particularly with 3rd line treatment

Promonstrual Syndrome Treatmont

Exercise, cognitive behavioural therapy,vitamin B» Vitex agnus castus(chasteberry)

First Line CMC

Continuous or luteal phase (day 15-28) low dose SSRIs(e.g. citalopram/escitalopram 10 mg)

Estradiol patches1100 pg) + micronised progesterone (100 mg or 200 mg [day 17-281,orally or

vaginally) or levonorgestrel-releasing intrauterine system (LNG-IUS) 52 mg

Higher dose selective serotonin reuptake inhibitors(SSRIs) continuously or in luteal phase

(e.g. citalopram/escitalopram 20-40 mg)

Second Line

Third Line f GnRH analogues add-back hormone replacementtherapy (HRT)

Fourth Line f Surgical treatment •HRT

Figure 5. Royal College of Obstetricians and Gynaecologists(RCOG) guidelines for treatment of premenstrual

syndrome

Adapted from source:Managementol Premenstrual Syndrome.Brit J ObstetGynaec 2016:48:1-33.

Premenstrual Dysphoric Disorder

Definition

• PMDD is similar to PMS but causes more severe symptoms and impairment of functioning

Clinical Features

• irritability and depressed mood

• breast pain and abdominal bloating

Diagnostic Criteria for Premenstrual Dysphoric Disorder

• at least 5 of the following 11 symptoms during most menstrual cycles of the last year (with at least I of

the first 4)

depressed mood or hopelessness

• anxiety or tension

• affective instability

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GY6 Gynaecology Toronto Notes 2023

anger orirritability'

decreased interest in activities

difficulty concentrating

• lethargy

change in appetite

hypersomnia or insomnia

» feeling overwhelmed

physicalsymptoms: breast tenderness/swelling, headaches, joint/muscle pain, bloating, or weight

gain

• symptoms cause significant distress and/or interfere with social or occupational functioning

• symptoms must be present during the week prior to menses and resolve within a few days after onset

of menses

• may be superimposed on other psychiatric disorders, provided it is not merely an exacerbation of

another disorder

Common Investigations and Procedures

Imaging

Ultrasound

• transabdominal or transvaginal U/S is the imaging modality of choice for pelvic structures

• transvaginal U/S provides better resolution of uterus and adnexal structures

detects early pregnancy if (5-hCG >1500 (|5-hCG must be >6500 for transabdominal U/S)

• may be used to identify pelvic pathology'

identify ectopic pregnancy, intrauterine pregnancy

assess uterine, adnexal, cul-de-sac, and ovarian masses (e.g.solid or cystic)

» determine endometrial thickness, locate/characterize fibroids

• detection of deep infiltrating endometriosis

• monitor follicles during assisted reproduction

assess endometrial lining in postmenopausal women

Endometrial Biopsy

• performed in the office using an endometrial suction curette (pipelle) guided through the cervix to

aspirate fragments of endometrium

• pre-treatment with misoprostol (Cytotec*) is optional (works better in premenopausal patients)

• more invasive procedure (i.e. D&C) may be done in the office or operating room ± hysteroscopy (this

may be required if endometrial biopsy is not possible in the office setting or if there is suspicion for an

endometrial polyp)

• indications

- AUB/PMB

age >40

risk factorsfor or history of endometrial cancer

failure of medical treatment

significant intermenstrual bleeding

consider in women with infrequent mensessuggesting anovulatory cycles

Hysterectomy No.377 - Hysterectomy forBenig n

Gyoaecological Indications

J Obstet Cyraecol Can 2019:41|4|:543-SS7

Summary:

1. Hysterectomy should be approached by either

vaginal, laparoscopic,oc open routes.

2.Correction of preoperatiieaaemia (hemi>globhi

(Hb <120 gfl). preoperatnre antibiotic prophylaxis,

and measures to decrease risk of venous

thromboembolism are recommended.

3.In patients with endometriosis,full excision

of local endometriosisshould be performed

(Oiarnvl v .

4.Opportunistic salpingectomy can be considered al

the time ol hysterectomy,but the planned surgical

approach should not be changed lor thissole

purpose.

5.Urinary tract injury is a known complication of

hysterectomy and there should be a low threshold

forfurther investigation in cases where injury is

suspected - consider routine cystoscopy.

6.Women should be counselled about the benefits

and risks of removing the ovaries, the risk

ol ovarian cancer vs.the long term health

Impllcotions ol earlier menopause.

Indications

• uterine fibroids

• endometriosis, adenomyosis

• uterine prolapse

• pelvic pain

• AUB

• cancer (endometrium, ovaries,fallopian tubes,cervix)

Complications

• general anesthetic

• bleeding

• infection

• injury to other organs (ureter, bladder, rectum)

• loss of ovarian function (if ovaries removed, iatrogenic menopause)

• venous thromboembolism +

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Approaches

1 . open (abdominal approach): uterus removed via transverse (Pfannenstiel) or midline laparotomy

2. minimally invasive approaches

vaginal hysterectomy: entire procedure performed through the vagina; no abdominal incisions

laparoscopic-assisted vaginal hysterectomy: vascular pedicles are divided by a combination of

laparoscopic and vaginal approaches

total laparoscopic hysterectomy: all vascular pedicles including the colpotomy approached

laparoscopically and removed through the vagina

robotic:a type of laparoscopic approach;may be advantageous in patients with a high BM1, but

more costly

Table 1. Classification of Hysterectomy

Classification Tissues Removed Indications

Subtotal Hysterectomy Inaccessible cervix (e.g. adhesions)

Patient choice/prelerence

Uterus, cervix,uterine artery ligated atuterus Uterine fibroids

Endometriosis

Adcnomyosis

Heavy menstrual bleeding

Uterus

TotalHysterectomy (TH)

(cxtralascial simple hystercctomy/type1)

DUB

TotalHysterectomy (TH)

(cxtralascial simple hystercctomy/type1)

and BilateralSalpingo-Oophorcctomy (BSO)

Modified Radical Hysterectomy(type 2) Uterus,cervix,proximal1/3 parametria. Cervical cancer (up tostage1B1)

uterine artery ligated medial tothe ureter,

midpoint of ulerosacral ligaments,and upper

1-2 cm vagina

Uterus, cervix,entire parametria,uterine Cervical cancer

artery ligated at its origin from internal iliac

artery,ulerosacral ligament at most distal

attachment (rectum),and upper 1/3-1/2 vagina

Uterus, cervix,uterine artery ligated at uterus. Endometrial cancer

lallopian lubes, ovaries Malignant adnexal masses

Consider lor endometriosis

Radical Hysterectomy (type 3)

Disorders of Menstruation

Amenorrhea

Differential Diagnosis of Amenorrhea Primary Amenorrhea

No menses by age13 in absence of 2°

sexual characteristics,or no menses by

age 15 with 2”

sexual characteristics,or

no menses 2 yr after thelarche

Table 2. Differential Diagnosis of Primary Amenorrhea

With Secondary Sexual Development Without Secondary Sexual Development

Normal Breast and Pelvic

Development

Normal 8reast,Abnormal

Uterine Development

High FSH

(Hypergonadotropic

Hypogonadism)

Low FSH

(Hypogonadotropic

Hypogonadism)

Secondary Amenorrhea

No menses for >6 mo or 3 cycles after

Hypothyroidism documented menarche

Hyperprolactinemia

PCOS

Hypothalamic dysfunction

Androgen insensitivity

Anatomic abnormalities

Mullerian agenesis,

uterovaginal septum,

impeilorate hymen

Gonadal dysgenesis

Abnormal sex chromosomes

(Turner's XO)

Normal sex chromosomes

(46XX. 4GXY)

Constitutional delay (rare in girls)

Congenital abnormalities

Isolated GnRH deficiency

Pituitary failure (Kallmann

syndrome,head injury,pituitary

adenoma,etc.)

Acquired endocrine disorders

(type 1DM)

Pituitary tumours

Systemic disorders (IBD.JRA.

chronic infections, etc.)

Functional hypothalamic

amenorrhea

Asherman'sSyndrome/uterine

defect

Most Common Causes of Primary

Amenorrhea

1 Gonadal dysgenesis (e.g.Turner's

Syndrome)

2. Functional hypothalamic amenorrhea

3. Mullerian agenesis

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Table 3. Differential Diagnosis of Secondary Amenorrhea

With Hyperandrogenism Without Hyperandrogenism

PCOS

Autonomous hyperandrogenism (androgen secretion independent of

the HPO axis)

Ovarian:tumour,hypcilhccosis

Adrenal androgen-secreting tumour

Late onset or mild congenital adrenal hyperplasia (rare)

Pregnancy

Hypergonadotropic hypogonadism (i.e.primary ovarian

insufficiency:high FSH,low estradiol)

Idiopathic

Autoimmune:type 1DM, autoimmune thyroid disease.Addison's

disease,celiac disease

Iatrogenic:cyclophosphamide drugs,radiation

Hyperprolactinemia

Endocrinopathies:most commonlyhyper or hypothyroidism

Hypogonadotropic hypogonadism(low ESH):

Pituitary compression or dcslrudron:pituitary adenoma,

craniopharyngioma,lymphocytic hypophysitis,infiltration

(sarcoidosis),head injury,Sheehan'ssyndrome

Functional hypothalamic amenorrhea (often related to stress,excessive

exercise and/or anorexia)

Functional hypothalamic amenorrhea is

the most common cause of secondary

amenorrhea

Amenorrhea

i

History and PhysicalExam

I

;

1'Amenorrhea 2 'Amenorrhea

I I

2sexual characteristics (3-hCG

^

No l

Negative

Prolactin

^

1

Yes Positive

Karotypc FSH/IH Pregnancy

1 1 t

I |

XY High

Hypergonadotropic

^

Hypogonadotropic

• Gonadal agenesis/ •Constitutional delay

* HPO axis abnormality

i

XX Lots Normal Abnormal

Imperforate hymen AIS

Transverse vaginal septum

Cervical agenesis

MOIIcrian agenesis

Prolactin t

(normal <20 ng/dl)

• CT head if >100 ng/dl

• TSHtoscroon

for hypothyroidism

Progesbn challenge

Withdrawal No withdrawal

bleed i

dysgenesis bleed

.

Primary ovarian

1

insufficiency

Uterine defect

Asherman’s syndrome

or HPO axis dysfunction

LH/FSH

I J

High Normal/Low

PCOS -hyperandrogenism HPO axis dysfunction

•MRI hypothalamus, pituitary

•Measure other pituitary hormones

•Common etiology:

•Weight loss

•Excessive exercise

• Systemic diseases

Figure 6. Diagnostic approach to amenorrhea

Investigations

• P-hCG, hormonal workup (1SH, prolactin, FSH, LH, androgens, estradiol)

• progesterone challenge to assess estrogen status

• medroxyprogesterone acetate (Provera*) 10 mg PO once daily for 10-14 d

• any uterine bleed within 2-7 d after completion of Frovera* is considered to be a positive W/L> test

• W/D bleed suggests presence of adequate estrogen to thicken the endometrium; thus W/D of

progesterone results in bleeding

if no bleeding occurs, this may be secondary to inadequate estrogen (hypoestrogenism),

excessive androgens or progesterones (decidualization), pregnancy, obstructive causes (e.g.

cervical stenosis), or structural causes (e.g. uterine adhesions)

• karyotype: indicated if primary ovarian insufficiency or absent puberty

• U/S to confirm normal anatomy, identify PCOS (in adult population only)

Prolactinoma Symptoms

Galactorrhea, visual changes,headache

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Treatment

Table 4. Management of Amenorrhea

Etiology Management

1° AMENORRHEA

Gonadal resection alter puberty

Psychological counselling

Creation ol neo- vagina with dilation

AIS

Anatomical

Imperforate hymen

Transverse vaginal septum

Cervical agenesis

Mullerian dysgenesis [MRKH syndrome)

Surgical management

Surgical management

Suppression and ultimately hysterectomy

Psychological counselling

Creation of neo vagina with dilation

Diagnostic study to confirm normal urinary system and spine

2

« AMENORRHEA

HPO axis dysfunction Identify modifiable underlying cause

Combined OCP to decrease risk ol osteoporosis, maintain normal vaginal and breast development

( NOT proven to work)

MRI/CT head to rule out lesion

If no demonstrable lesions by MRI:

Bromocriptine, cabergoline if fertility desired

Combined OCPs il no fertility desired

Demonstrable lesions by MRI: surgical management

See PolycysticOvarian Syndiome, CY 24

Screen foi DM , hypothyroidism, hypoparathyroidism, hypocortisolism

Hormonal therapy with estrogen and progestin to decrease risk of osteoporosis:can use OCP

after induction of puberty

Evaluation with hysterosalpingography or sonohysterography

Hysteroscopy:excision ofsynechiae

Hyperprolactinemia

2° amenorrhea is pregnancy until proven

otherwise

Polycystic ovarian syndrome

Premature ovarian failure

Uterine defect

Asherman'

ssyndrome

Abnormal Uterine Bleeding

AUB

i

T

Regular

( predictable cycle)

Irregular

(unpredictable cycle)

AUB and/or

Heavy Intermenstrual Bleeding unpredictable AUB

AUB-0

AUB-M

AUB-A

AUB-Uv

AUB-C

AUB-E

AUB-P

Figure 7. Diagnostic approach to abnormal uterine bleeding

Approach

•menstrual bleeding should be evaluated by ascertaining: frequency/regularity of menses, duration,

volume of flow, impact on quality of life, and timing ( inter- or premenstrual, or breakthrough)

•is it regular?

regular: cycle to cycle variability of <20 d -

“Can you predict your menses within 20 days?

"

irregular: cycle to cycle variability of >20 d

•is it heavy?

questions: How frequently do pads/tampons need to be changed? How saturated? Any clots?

S80 cc of blood loss per cycle or

• S8 d of bleeding per cycle or

bleeding that significantly affects quality of life

Postmenopausal bleeding Is endometrial

cancer until proven otherwise

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Abnormal Uterine Bleeding

Change in frequency, duration,or

amount of menstrual flow that affects

quality of life

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• is it structural?

• PALM (see Table 5)

• is it non-structural?

COLIN (see Table5)

Table 5. Abnormal Uterine Bleeding - Etiologies, Investigations, and Management

Etiology Investigations Management

STRUCTURAL

Transvaginal sonography

Saline infusion sonohysterograpny

Transvaginal sonography

Polyps (AUB-P) Polypectomy (triage based on symptoms,

polyp sire, histopathology, and patient age)

Adenomyosis ( AUB- A ) See Adenomyosis, 6H3

MRI

leiomyoma ( AUB- L)

Submucosal (AUB-Lsm)

Other (AUB- Lo)

Transvaginal sonography

Saline inlusion sonohysterography

Diagnostic hysteroscopy

See fibraidi, 014

MRI

Malignancy and Hyperplasia (AUB- M ) Transvaginal sonography

Endometrial biopsy (or all women > 40 yr with

AUB. lor women * 40 yt with persistent AUB. or

endometrial cancer nsh factors

Dependent on diagnosis

NON-STRUCTURAl

CBC, coagulation profile (especially in

adolescents),VWF. Ristocetin cofactor,

factor VII

Bloodwotk: p hCG.ferritin, prolactin, FSH. IH.

serum androgens(free testosterone, DHEA).

progesterone,17-hydroxy progesterone.ISH,

free T4

Pelvic ultrasound

Endometrial biopsy

Coagulopathy (AUB-C) Dependent on diagnosis (hormonal modulation

(e.g. OOP).Mirena IUS. endometrial ablation)

Ovulatory Dysfunction (AUB 0) See Inltthlilf,6K23

Endometrial (AUB E) Traneramicacrd

Hormonal modulation (e.g, OCP)

Mirena IUS

Endometrial ablation

Iatrogenic (AUB-I ) Transvaginal sonography (rule out forgotten Remove offending agent

IUD)

Review OCPfHRT use

Review medications(especially neuroleptic

use)

Not VetClassified (AUB N )

Treatment

• resuscitate patient if hemodynamically unstable

• treat underlying disorders

• if anatomic lesions and systemic disease have been ruled out, consider AUB

• medical

mild AUB

NSAIDs

anti-fibrinolytic (e.g.Cyklokapron*) at time of menses

combined hormonal contraceptive

progestins(Provera*) on first 10-14 d of each month or every 3 mo if AUB-0

Mirena* IUD

correct anemia - iron

acute,severe AUB

replace fluid losses, consider admission

a) estrogen (Premarin*) 25 mg IV q4 h x 24 h with Gravol* 50 mg IV/PO |c 4 h or anti

-

fibrinolytic (e.g.Cyklokapron") 10 mg/kg IV q8 h (rarely used)

b) tapering OCP regimen, 35 pg pill T1D x 7 d then taper to 1 pill/d for 3 wk with Gravol* 50

pg IV/PO q4 h

- or taper to 1 tab T1D x 2 d •> BID x 2 d -> once daily (more commonly used)

after (a) or (b), maintain patient on monophasic OCP for next several months or consider

alternative medical treatment

- medical (can also consider):

- high dose progestins

- danazol (Danocrine*)

- GnRH agonists(e.g. Lupron * ) with add-back if taken for >6

- ulipristal acetate

mo r m

l i

- J

• surgical

polypectomy

myomectomy

* uterine artery embolization

endometrial ablation

+

• if finished childbearing

• repeat procedure may be required if symptoms recur, especially If <40 yr

• hysterectomy: definitive treatment

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Dysmenorrhea

Etiology

• primary/idiopathic

• secondary (acquired)

• endometriosis

adenomyosis

uterine polyps

uterine anomalies(e.g. non-communicating uterine horn)

leiomyoma

• intrauterine synechiae

• ovarian cysts

• cervical stenosis

Primary Dysmenorrhea

Recurrent,crampy lower abdominal

pain during menses in the absence of

demonstrable disease

Secondary Dysmenorrhea

Pain during menses that can be

attributed to an underlying disorder (i.e.

endometriosis,adenomyosis.fibroids)

imperforate hymen, transverse vaginal septum

rlD

IUD (copper)

foreign body

Table 6. Comparison of Primary and Secondary Dysmenorrhea

Primary Dysmenorrhea Secondary Dysmenorrhea

Recurrent,crampy lower abdominal pain that occurs Similar features as primary dysmenorrhea but with an

during menses in the absence ol demonstrable disease underlying disorder that can account for the symptoms.

such as endometriosis,adenomyosis.or uterine fibroids

Colicky pain in abdomen,radiating to the lower back. Same symptoms as primary dysmenorrhea

labia,and inner thighs beginning hoursbefore onset of Associated symptoms:dyspareunia,abnormal bleeding.

bleeding and persisting for hours or days (48-72 h) infertilily

Associated symptoms:N/V, altered bowel habits,

headaches, fatigue (prostaglandin-associated)

Assess for associated dyspareunia.abnormal bleeding. Bimanual exam:uterine or adnexal tenderness,fixed

infertility (signs of 2’

dysmenorrhea)

Buie out underlying pelvic pathology and confirm cyclic or enlargedirregular uterus (findings are rare in women

nature of pain

Pelvic examination not required;indicated for patients U/S.laparoscopy,end hysleroscopy may benecessary to

not responding to therapy or with signsof organic establish the diagnosis

pathology Vaginal andcervical cultures may be required

Regular exercise,local heat

NSAIDs:should be startedbefore onset of pain

CHCs with continuous or extended use: suppress

ovulation/reduce menstrual flow

Features

Signs andSymptoms

Diagnosis

uterine retroflexion,uterosacral nodularity,pelvic mass.

<20 yr)

Treatment Treatunderlying cause

Endometriosis

Definition

• the presence of endometrial tissue (glands and stroma) outside of the uterine cavity

• chronic condition, resolving only with menopause

Etiology

• not fully understood; proposed mechanisms include (combination likely involved):

• retrograde menstruation (Sampson’s theory)

immunologic:decreased N K cell activity limiting clearance of transplanted endometrial cells

from pelvic cavity (may be due to decreased N K cell activity)

metaplasia of coelomic epithelium

• extra- pelvic disease may he due to aberrant vascular or lymphatic dissemination of cells

• e.g. ovarian endometriosis may be due to direct lymphatic flow from uterus to ovaries

Epidemiology

• incidence: 15-30% of premenopausal women

• mean age at presentation: 25-30 yr

• regresses after menopause

Risk Factors

• family history (7-10x increased risk if affected 1st degree relative)

• obstructive anomalies of the genital tract (earlier onset) -resolves with treatment of anomaly

• nulliparity

• age >25 yr

• early menarche (<11-13 years old),shorter menstrual cycles (defined as <27 days)

Differential Diagnoses

• Chronic PID,recurrent acute

salpingitis

. Hemorrhagic corpus luteum

• Bcnign/malignant ovarian neoplasm

• Ectopic pregnancy

4 “Dys" of Endometriosis

• Dysmenorrhea

• Dyspareunia (cul-de-sac,uterosacral

ligament)

• Dyschezia (uterosacral ligament culde-sac.rectosigmoid attachment)

• Dysuria (bladder involvement)

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Sites of Occurrence

• ovaries: 60% of patients have ovarian involvement

• broad ligament, vesicoperitoneal fold

• peritoneal surface of the cul-de-sac, uterosacral ligaments

• rectosigmoid colon, appendix

• rarely may occur in sites outside abdomen/pelvis, including lungs and diaphragm

Long-Term Outcomes of Elagolix in Women with

Endometriosis:Resultsfrom Two Extension

Studies

Obstet Gynecol 2018:132.147-160

Purpose: An evaluation of the safety and efficacy of

elagolix (a GnRH agonist)orer 12 mo in women wdh

endometriosis-associated pain.

Methods A repwlof 2. double - blind. Phase III.

placebo-controlled Misto evaluate (wo doses

ol elagolix over 12 mo of continuous treatment m

patients with moderate lo severe endometriosisassociated pain.

Results: In the lint trial.S2.1lol women receiving

ISO mg elagot'ionce daily had a dincal response

with regards lo dysmenorrhea and 67.8% had a

response with regardslo coo-menstrual pelvic pain.

In tine h gher dose group (200 mg q12 h),the response

rate was 78.1% and 69.1%.respectively,these

response rateswere comparable in the second trial.

Women who received elagb ix had higher rates of hot

flushes, higher serum I puts,and deueasesin hone

mineral density.

Conclusion : Both h gb and low doses of elagolix

were effective m improving dysmenorrhea and non- menstrual pelvic pain in women with endometriosisassociated pain.

Clinical Features

• may be asymptomatic and can occur with one of 3 presentations

I. pain (80%)

• menstrual symptoms

cyclic symptoms due to growth and bleeding of ectopic endometrium, usually precede

(24-48 h ) and continue throughout and after flow

menses

secondary dysmenorrhea

sacral backache with menses

pain may eventually become chronic, worsening perimenstrually

deep dyspareunia

bowel and bladdersymptoms

frequency, dysuria, hematuria

cyclic diarrhea/constipation, hematochezia, dyschezia (suggestive of deeply infiltrating

disease)

2. infertility (25%)

30-40% of patients with endometriosis will be infertile

• 15-30% of those who are infertile will have endometriosis

3. mass (endometrioma) (20%)

• endometrioma:an endometriotic cyst encompassing ovary

ovarian mass can present with any of above symptoms or be asymptomatic

physical examination:

tender nodularity of uterine ligaments and cul-de-sac felt on rectovaginal exam

fixed retroversion of uterus

firm,fixed adnexal mass

Investigations

• definitive diagnosis can be made based on:

direct visualization of lesions typical of endometriosis at laparoscopy ( gold standard)

• biopsy and histologic exam of specimens 2 or more of: endometrial epithelium, glands,stroma,

hemosiderin-laden macrophages

• laparoscopy

mulberry spots:dark blue or brownish-black implants on the uterosacral ligaments, cul-de-sac, or

anywhere in the pelvis

endometrioma:

“chocolate"

cysts on the ovaries

“powder-burn" lesions on the peritonealsurface

early white lesions and clear blebs

peritoneal “pockets"

• CA-125

maybe elevated in patients with endometriosis but should NOT be used as a diagnostic test

Endometriosis- Take Home Points

• Suggestive history even with a

negative exam should be considered

adequate for a presumptive

diagnosis

• Pelvic pain that is not primary

dysmenorrhea should be considered

endometriosis until proven otherwise

• Medical management is the mainstay

of endometriosis

Suspocted Endometriosis

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First Line

CHC therapy (ideally continuous!

Progestin alone (oral. IM, SC)

Failure of first line therapy

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Second Line

1. GnRH agonist with addback

2. Progestin IUS

Laparoscopy for u.

diagnosis and treatment Failure of surgical or

medical therapy

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