dysmenorrhea and endometriosis Flashcards
A 26 yo law student, G0 LMP 2 weeks ago c/o constant and severe dysmenorrhea beginning on the first day of menses x 2 years. She states the severity of the dysmenorrhea is worsening. She sometimes has to miss class due to the pain as well as the fact that sometimes she faints from the severity of the pain. Her sister was recently diagnosed with endometriosis. She finds no relief from naproxen (Aleve). She wonders if she should try birth control pills.
She recently consulted a gynecologist who is well respected in the field of dysmenorrhea. The physician told the patient that her pain was due to anxiety and that she needed to consult a psychotherapist.
Your patient tries extended cycle oral contraceptives with minimal improvement of her dysmenorrhea. She undergoes laparoscopy with excision of all visible endometriosis, and then begins leuprolide thereafter. She notes significant improvement in her symptoms within 4-8 weeks after surgery.
primary dysmenorrhea
-80% of all patients at some point in reproductive life
-Caused by prostaglandin secretion
-No underlying pathology
-Is not disabling or incapacitating
-Clinical diagnosis based on history alone
-No findings on physical exam
-No need for imaging or other ancillary testing
-Treat with NSAID of choice
secondary dysmenorrhea
-caused by some type of underlying disorder
-common etiologies:
-Endometriosis- Ectopic deposits of endometriotic tissue
-Leiomyomata uteri- Benign tumors of uterus composed of smooth muscle
-Adhesions
-Adenomyosis- Endometriosis within myometrium
-Imperforate hymen
-Cervical stenosis
-other processes involving GI, GU, MSK, and neuro
endometriosis definition and incidence
-Ectopic deposits of endometrial tissue that appear in other parts of the body, most commonly in the pelvis
-Myometrium, tubes, ovaries, vagina, rectum, etc.
-Occurs in 10% of all patients assigned female at birth
-Causes chronic pelvic pain and infertility
endometriosis
-MCC of chronic pelvic pain in women of reproductive age
-inflammatory process that requires estrogen to continue
-estrogen receptor beta increases survival of endometriotic lesions and also affects inflammatory response so that pain is increased
-progesterone resistance occurs due to few progesterone receptors in endometriotic lesions
endometriosis risk factors
-Early menarche
-Short cycles (<27 days)
-Heavy menses
-Tenfold increase in patients with 1st degree relative with endometriosis
-Also increased in patients with imperforate hymen
-Found in large percentage (up to 30-40%) of patients having laparoscopy for pelvic pain or for infertility
-However, this is not known to be a causal association
endometriosis pathophysiology
-3 theories have existed for many years:
-Sampson’s theory
-Direct implantation of endometriotic tissue due to retrograde menstruation; malignant transformation suggested by Sampson in 1925
-Halban’s theory
-Vascular or lymphatic dissemination of endometrial cells
-Explains distant involvement (pleurae, kidney, etc.)
-Meyer’s theory
-Coelomic metaplasia of multipotential cells in peritoneal cavity
-However, gene mutation is also part of the etiology of endometriosis
-local overproduction of prostaglandins through increase in COX-2 activity
-overproduction of local estrogens by increased aromatase activity
-progesterone resistance reduces the antiestrogenic effect of progesterone and increases local estrogen effect
pathophysiology of pain assoc with endometriosis
-Endometriotic lesions produce chronic inflammation:
-Proinflammatory cytokines (tumor necrosis factor α and interleukins)
-Pain occurs in part due to the increase in prostaglandins
-Chronic inflammation is thought to:
-Increase in nerve growth, particularly in rectovaginal lesions
-Increase in density of nerve fibers, particularly in deep lesions
-Changes in uterine innervation
association of infertility with endometriosis
-probably due to cytokines:
-may also affect sperm by causing DNA damage
-may cause damage to oocyte cytoskeletons
-other results in tubal damage
endometriosis: pain, GI sx, bladder, MSK, other
-Pain:
-dysmenorrhea
-Chronic pelvic pain (pelvic pain on more days than not for at least 6 months with no known etiology)
-Deep dyspareunia (especially perimenstrual dyspareunia)
-GI sx:
-Perimenstrual tenesmus
-Perimenstrual dyschezia
-Perimenstrual hematochezia
-Perimenstrual diarrhea or constipation
-Bladder: perimenstrual dysuria
-MSK- back pain
-Other- near syncope or syncope
physical exam findings: endometriosis
-classic findings:
-uterosacral nodularity on recto vaginal exams, but it is frequently not present
-endometriomas may be present
-however, in reality- uterosacral nodularity may not be appreciated or present
dx of endometriosis
-At this time, it may be suspected and dx presumptively, but can be proved only through direct visualization in surgery or through bx
-May find endometriotic implant in lower genital tract in luteal phase
-May biopsy lesion
-Though pelvic ultrasound is of limited benefit, it should be performed in all patients with secondary dysmenorrhea to rule out other processes and to identify endometriomas
-The FDA has fast tracked a new test for superficial peritoneal endometriosis with a radio-labeled tracer that would be of use in patients 16 years of age and older
-SPE is considered to be the earliest form of endometriosis
laparoscopy
-Minimally invasive surgery used in the abdomen
-Small incisions are used rather than a large incision
-May be diagnostic only, or may involve treatment as well
-Generally uses carbon dioxide to create pneumoperitoneum
-Protects peritoneal cavity from potential perforation at insertion of trocars
-While assoc with less postoperative pain and faster recovery, it usually takes longer than an open procedure
-This may increase risk of:
-Sepsis
-Atelectasis
-Pneumonia
-Deep vein thrombosis
endometriosis: findings at surgery
-Small, dark red lesions
-May be described as “powder burn” or “mulberry” lesions
-Endometriomas filled with dark red or brown fluid
-“chocolate cysts”
-Most commonly involves
-Surface of uterus
-Tubes
-Ovaries
-Pouch of Douglas
-Uterosacral ligaments, round ligament, tubes, sigmoid, rectovaginal septum
-Can involve practically any structure in body
endometrioma
-chocolate cyst
classification of staging of endometriosis via American Society for Reproductive Medicine (ASRM)
initial medical management of endometriosis in pts with pain and who are desirous of future fertility
-NSAIDs with oral contraceptives, AND with oral or depot medroxyprogesterone acetate, OR
-Progestins
-GnRH agonists
-Androgens
-Consider strongly the use of extended cycle OCs
medical management of endometriosis in pts with pain and with infertility
-Surgery does improve potential for fertility, but the improvement has not yet been measured
-Surgical interventions: Excision of endometriomas
-If infertility is not improved after surgery, proceed to in vitro fertilization
management of pts in whom initial medical therapy for pain has failed
-GnRH therapy for up to 12 months
-GnRH antagonists
-Elagolix
-Relugolix
-Aromatase inhibitors AND progestin OR combined OC
-Decreases FSH release
-May combine with oral contraceptive or progestin, such as norethindrone acetate
-“Insufficient data to recommend use” (ACOG)
-Selective progesterone receptor modulators:
-Mifepristone
-Asoprisnil
-Ulapristal
-NSAIDs- selective COX-2 inhibitor (celecoxib)
surgical management of endometriosis
-Conservative:
-Excision or ablation of all visible disease
-Adhesiolysis, if needed- May be helpful to treat with medical Rx before and after sx
-May also perform presacral neurectomy for midline pain, if indicated- May cause urinary dysfunction and constipation
-Extirpative:
-Total abdominal hysterectomy and bilateral salpingo-oophorectomy (BSO) v USO if both ovaries are not involved -> Salpingectomy should be performed when a patient is having a hysterectomy
-Ovarian conservation increases risk of recurrence but also reduces risk of osteoporosis -> Increased longevity is also associated with ovarian conservation
Association with malignancy
-Gene mutations associated with both endometrial and ovarian carcinoma are also associated with endometriosis
-ARID1A (tumor suppressor) gene mutation
-PIK3CA gene mutation- An instructional gene that, when affected by mutation, leads to uncontrolled growth
-Endometriomas seem to serve as a precursor to development of ovarian carcinoma
-ovarian endometriosis is assoc with endometrioid and clear cell ovarian carcinoma
-women with endomtriosis have an increased risk of ovarian carcinoma (odds ratio: 1.46)
-Prevention is the only method of management -> No adequate screening method currently exists
-Excision of all visible endometriotic implants is currently the best method of preventing ovarian carcinoma in women with endometriosis -> Alternatively, hormonal therapy with oral contraceptives or other hormones may be used
-Salpingectomy may reduce the risk of ovarian carcinoma by 40%
infertility
-IVF is the preferred management in pts with infertility and endometriosis
