Pocket Obstetrics and Gynecology

GENERAL GYNECOLOGY

VULVOVAGINITIS

Definition (Obstet Gynecol 2006;107:1195)

• Vulvovaginal sx such as itching, burning, irritation, & abn discharge d/t various causes. BV = Most common (MCC), vulvovaginal candidiasis, & Trichomonas vaginalis.

• Nml vaginal flora: ↑ estrogen → ↑ vaginal epithelial glycogen → ↑ gluc source → ↑ lactobacilli → ↑ lactic acid → ↓ vaginal pH @ 3.8–4.5 (NEJM 2006;355:1244)

Pathophysiology & Risk Factors

Clinical Manifestations (NEJM 2006;355:1244)

• BV: Copious, thin, whitish-gray, fishy-smelling discharge. Less likely pruritus.

• Candidiasis: Thick, white, curdy discharge. No odor. + Pruritus, dysuria, vaginal erythema.

• Trichomonas: Copious yellow to greenish, frothy discharge. Often foul odor. ± pruritus, postcoital bleeding, dysuria. ± vaginal or cervical erythema (“strawberry cervix”).

Diagnostic Studies (NEJM 2006;355:1244)

• BV: Nugent score = gold std, gram stain w/ scored bacteria & clue cells.

• Candidiasis: Presence of hyphae visible on KOH or wet mount. Yeast cx useful if pt c/o sx but negative wet mount, or if recurrent infxns.

• Trichomonas: Presence of mobile trichomonads on wet mount; ↑ PMNCs often present.

Treatment

BARTHOLIN GLAND CYST AND ABSCESS

Definition (J Obstet Gynaecol 2007;27:241)

• Bartholin gland secretes mucous vaginal lubrication. Located at ∼4- & 8-o’clock on labia minora bilaterally. Not palpable unless pathology. Usually women b/w 20–30 yo.

Etiology & Pathophysiology

• Blockage of gland outflow → accum of mucous → Bartholin duct cyst.

• Superficial infxn of a Bartholin cyst → Bartholin duct abscess. Polymicrobial. Most common bacteria are anaerobic & facultative aerobes.

• Bartholin cyst & abscess uncommon >40 yo. Consider biopsies of cyst wall to r/o cancer.

Clinical Manifestations and Physical Exam

• Small cysts are asx. Larger → vaginal pres or dyspareunia. Typically unilateral, round, & tense.

• Abscess = sev pain → difficulty walking, sitting, engaging in sex. May be tender w/ erythema/induration, purulent drainage.

• DDx: Epidermal inclusion cysts, mucous cyst of vestibule, cyst of canal of Nuck, Skene’s duct cyst (J Obstet Gynaecol 2007;27:241)

Treatment (See also Appendix of Common Procedures)

• Small, asx cyst requires no rx. OTC analgesics, warm compresses, & sitz baths may provide sx relief.

• Abscess may drain spontaneously. Immediate pain relief will occur w/ drainage.

• Surgical mgmt reserved for recurrences, abscesses, or large symptomatic cyst.

(1) I&D: Relief but incision can reseal → reaccumulation of fluid. Word catheter (or pediatric Foley) allows continued drainage & tract epithelialization. High recurrence rates after I&D. Leave catheter 4–6 w. May fall out before then.

(2) Marsupialization: Create new drainage site. Incise roof of cyst → sew edges of cyst wall to adj skin edge. Requires anesthesia, ↑ time, & placement of sutures. Low recurrence after marsupialization.

(3) Bartholin gland excision: Reserved for cyst that recurs repeatedly. ↑ risk of bleeding. Not performed if active infxn.

Antibiotic therapy often prescribed after surgical rx. Cx rarely change mgmt (Am Fam Physician 2003;68:135). Use broad spectrum abx, failure of clinical improv, consider MRSA.

UTERINE FIBROIDS

Definition

• Benign smooth muscle tumors, originating from myometrial tissue (leiomyoma).

• Uterine fibroids can be classified based on their anatomical location.

Epidemiology (Obstet Gynecol Clin N Am 2011;38:703)

• By 50 yo, fibroids are found in ∼70% of whites & >80% of blacks. Indication for 30–40% of hysterectomies. Risks: >40 yo, black, FHx, nulliparity, obesity.

Pathology

• Gross: Pearly, round, well circumscribed. Size & location vary. Relatively avascular but surrounded by rich vasculature system → signif bleeding.

• Histology: Smooth muscle cells aggregated in bundles.

• Degenerating leiomyoma types: Hyaline (65%), myxomatous (15%), calcific (10%, mainly older women), cystic (4%, hylanized areas → liquefaction), fatty (rare), carneous (red) necrosis (esp pregnantpts, acute d/t outgrowing bld supply → acute musc infarction → sev pain & local peritoneal irritation).

• Leiomyomas do not transform into leiomyosarcoma. Likely represents a de novo neoplasm & is NOT a result of malig transformation of a benign tumor.

Figure 5.1 Fibroid location & nomenclature

Pathophysiology

• Fibroids are estrogen- (& progesterone-) sensitive tumors. Fibroids create ↑ estrogen environment → ↑ growth & size maint. ↑ estrogen conditions (obesity, early menarche) → ↑ fibroid risk.

Clinical Manifestations

• Mostly asx. Sx depend on size, location, & number. In general, the larger the fibroid, the larger the chance of sx.

• Vaginal bleeding = most common symptom; usually presents as menorrhagia.

• Other sx: Pelvic pain & pres, urinary frequency, incontinence, constip, infertility

• Evid sugg that myomas are the primary cause of infertility in a small # of women. Myomas that distort the uterine cavity & larger intramural myomas may have adverse effects on fertility (Fertil Steril2008;90:S125).

Physical Exam & Diagnostic Studies

• Findings: Uterine enlargement, irreg uterine contour.

• Must r/o other causes of abn bleeding. Postmenopausal bleeding w/ fibroids should be evaluated the same way as women w/o fibroids.

• Imaging:

US: Defines pelvic anatomy & effective in locating fibroids.

SIS: Allows eval of uterine cavity, particularly if infertility or menorrhagia is a concern. Good for submucosal type.

MRI: Very accurate. Very expensive. Not practical depending on the clinical setting.

Hysteroscopy: Gold std for submucosal fibroid.

Treatment & Medications

• Observation: Asx fibroids do not require intervention, no matter their size.

• Medical mgmt (Obstet Gynecol Clin N Am 2011;38:703): Should be tailored to alleviating sx. Cost & s/e of rx may limit long-term use.

NSAIDs: No data to support use as sole agent for therapy. Good for dysmenorrhea based on role of PGs as pain mediators.

OC: 1st line. Combined OCs may control bleeding & pain, but progestin-only OCs w/ mixed results.

Levonorgestrel IUD: Beneficial for menorrhagia. ↑ rate expulsion & vaginal spotting.

GnRH agonist (Leuprolide 3.75–11.25 mg/m IM): Reversible amenorrhea in most, & 35–65% ↓ in size w/i 3 mo. Most useful in women w/ large fibroids. Induces menopause sx + ↓ bone density. Consider add-back therapy for prolonged use (>6 mo) or symptomatic pts. Use preop → ↓ uterine size before Surg.

Aromatase inhibs: Block ovarian & periph estrogen production → ↓ estradiol level after 1 d of rx. ↓ s/e compared to GnRH w/ rapid results. Little data.

Antiprogestins (Mifepristone 5 or 10 mg/d ¥ 6 mo): 26–74% ↓ in uterine vol & ↓ recurrent growth after cessation. S/e: Endometrial hyperplasia (dose-dependent) & transient ↑ in transaminase (monit LFTs).

• Nonsurgical mgmt:

UAE: IR injects PVA spheres into bilateral uterine artery → ↓ bld flow → ischemia & necrosis → ↓ size & sx. Postembolization syn may require hospitalization postop for pain control. Successful pregnancies occur after UAE, but long-term data limited.

US ablation under magnetic resonant guidance:

• Surgical Mgmt:

Hysteroscopic myomectomy: 1st line for symptomatic submucosal fibroids.

Myomectomy: Option for those desiring fertility or decline hysterectomy. Goal to remove visible & accessible fibroids, & reconstruct uterus. Via laparotomy or laparoscopy. Fibroids may recur. When myomectomy invades endometrial cavity (complete wall resxn) consider CS deliv @ 37–38 w gest (Obstet Gynecol 2011;118:323).

Hysterectomy: Definitive surgical rx. Satisfaction rate >90%.

ADENOMYOSIS

Definition & Pathogenesis

• Presence of endometrial glands & stroma w/i the uterine musculature

• Amt & degree of invasion vary. Diffuse or circumscribed focal glandular deposits.

Epidemiology

• Unclear etiology, but several theories. Possibly invagination of endometrium into myometrium, or misplaced stem cells or Müllerian remnants.

• 70–80% of cases seen in 4th & 5th decades. Only 5–25% of adenomyosis seen <39 yo.

• Estrogen & progesterone likely play role in dev & maint. Often develops during reproductive years & regresses after menopause. Risk factors: Parity, ↑ age

Clinical Manifestations & Physical Exam Findings

• Menorrhagia & dysmenorrhea. Many asx. Severity correlates w/ ↑ ectopic foci & extent of invasion. Less common complaints: Dyspareunia, CPP, infertility.

• Ectopic endometrial tissue → proliferates → enlarged globular uterus on exam

Diagnostic Workup (J Minim Invasive Gynecol 2011;18:428)

• Dx by histology. Uniform dx based on histology not yet developed.

• ↑ Ca-125 levels may be seen, but not proven to be helpful in mgmt or dx.

• TVUS preferred imaging technique = ill-defined myometrial heterogeneity, may be myometrial cysts (round anechoic areas). MRI may be complementary = large asym uterus, thickened junctional zone (innermost myometrial layer), no fibroids.

Treatment & Medications

• No medical therapy exists at this time to treat sx while allowing pts to conceive.

• Conservative, medical mgmt for symptomatic adenomyosis similar to 1° menorrhagia or dysmenorrhea. Goal = temporarily induce regression of adenomyosis.

• NSAIDs often given. May consider: Continuous oral contraceptives, progestins, Mirena IUD, danazol, & GnRH agonist.

• Surgical Mgmt (J Minim Invasive Gynecol 2011;18:428):

Hysterectomy = Std rx option for those done w/ childbearing.

Endometrial ablation = Treats menorrhagia sx. Less successful if ↑ penetration of adenomyosis into uterus is present.

UAE: Controversial. Less successful if fibroids also present.

Focal excision: Must be able to identify area, margins, & extent of dz. Low efficacy (50%). Addition of GnRH agonist ↓ relapse rates by 20% in 2 y. May have fertility & deliv implications depending on size & location of excision.

ENDOMETRIOSIS

Definition and Epidemiology (Obstet Gynecol 2011;118:69)

• Defined as presence of endometrial glands & stroma outside of nml location in uterus.

• Hormonally dependent → mostly reproductive aged women (6–10 prevalence %).

• Prevalence of 38% in infertile women & 71–87% w/ CPP.

• Risk factors: Early menarche (<11 yo), menstrual cycles <27 d, heavy & prolonged menses.

• Protective factors: ↑ parity, ↑ lactation periods, regular exercise (>4 h/w).

Etiology

• Most commonly accepted theory = retrograde menstruation → attachment of endometrial tissue on peritoneum. Other theories: Bld or lymph transport, stem cells from bone marrow, coelomic metaplasia.

Clinical Manifestations (Obstet Gynecol 2011;118:69)

• Often asymptomatic. Common: Dysmenorrhea, CPP, menorrhagia, dyspareunia.

• Pelvic pain described as pain before onset of menses (2° dysmenorrhea), deep dyspareunia (worse during menses), sacral backache during menses.

Diagnostic Workup/Studies (N Engl J Med 2010;362:2389)

• Physical exam findings: Uterosacral ligament nodularity, adnexal mass

• Laparoscopy w/ or w/o bx for histology (gold std). Path: Endometrial glands/stroma w/ varying amts of inflammation/fibrosis. Bld or hemosiderin-laden macrophages. Bx not req, but definitive.

• Visual appearance: Classical lesions = black powder burn. Nonclassical = red or white.

• No correlation b/w severity of visual dz & degree of pain or prog w/ rx.

• No serum markers or imaging studies useful in dx. Imaging studies (MRI, USG) only useful if + pelvic/adnexal mass (chocolate cyst).

• US: Ovarian endometriomas appear as cyst w/ low-level, homogenous internal echoes from old bld. TVUS = imaging of choice to detect deeply infiltrating endometriosis of rectum or rectovaginal septum. MRI rarely req.

Classification

• Numerous schemes proposed. ASRM classification most common. Value = uniform recording of OR findings & comparing therapeutic interventions.

• ASRM criteria: Stage I (minimal) → Stage IV (sev). Based on extent & location of endometriosis lesions seen during operative procedure.

Treatment & Medications

• Best treated medically w/ surgical backup. Surgical mgmt reserved for large endometriomas, palpable dz, or infertility (Fertil Steril 2008;90:S260).

Figure 5.2 Management algorithm for endometriosis

• Medical therapy (Fertil Steril 2008;90:S260): Medical suppressive therapies are ineffective for infertility (Int J Gynaecol Obstet 2001;72:263)

NSAIDs: COX inhibs → ↓ PG synthesis → ↓ pain & inflammation

OCs: Can be used in cyclic or continuous fashion. Amenorrhea often result of continual therapy, which is often beneficial for pt w/ pain sx.

Progestins: Antagonize estrogenic effects on endometrium → decidualization → eventual endometrial atrophy.

Medroxyprogesterone acetate 20–100 mg PO QD or 150 mg IM q3mo (depot)

NETA 5 mg QD, ↑ 2.5 mg QD until amenorrhea or → 20 mg/d max reached

Mirena IUD. Unk MOA. Is efficacious, but not approved by FDA for this use.

GnRH agonists: ↓ signaling of HPA-axis → ↓ estrogen → amenorrhea & endometrial atrophy. Nasal spray (nafarelin acetate) or depot formulation (leuprolide acetate) q1–3mo. S/e = menopause sx + ↓ bone density. Add-back therapy w/ progesterone or combo (estrogen/progesterone) used to ↓ s/e. Theory = amt necessary to prevent menopause sx < amt to stimulate endometriosis. Can be started immediately w/ GnRH agonist administration. Does not diminish efficacy of pain relief. Norethindrone acetate (only hormone FDA approved for add-back therapy) 5 mg PO QD w/ or w/o CEE (premarin) 0.625 mg QD × 12 mo.

Danazol (600–800 mg QD): Inhibit LH surge → chronic anovulatory state. Substantial androgenic & hypoestrogenic s/e that limit clinical utility.

Aromatase inhibs: Still investigational. Not definitive therapy.

• Surgical therapy (Fertil Steril 2008;90:S260): Relief of pain after surgical rx = 50–95%. Laparoscopic rx of visible endometriosis improves pain. All visible lesions should be treated.

Conservative Surg (diagnostic laparoscopy, lysis of adhesions, ablation/fulguration of visible implants, normalization of anatomy) = 1° approach for symptomatic or large endometriomas b/c medical therapy will not lead to complete resolution. Cyst excision in endometriomas has improved outcomes over simple cyst drainage.

LUNA: Disrupts efferent nerve fibers in the uterosacral ligaments → ↓ uterine pain for intractable dysmenorrhea. No benefit > conservative Surg alone.

Presacral neurectomy: Interrupts symp innervation to uterus @ level of superior hypogastric plexus. Benefit in midline pain only. Technically challenging w/ signif risk of bleeding. S/e: Constip, urinary dysfxn.

Hysterectomy (TAH/BSO): For those w/ debilitating sx, have completed childbearing, & failed other therapies. Long-term adherence w/ HRT req to prevent ↑ risk of mortality a/w BSO prior to menopause (Obstet Gynecol2010;116:733). Use estrogen/progesterone therapy d/t risk of unopposed estrogen more likely to cause growth of endometrial implants.

• Surg, followed by medical therapy offers longer sx relief than w/ Surg alone. OC, progestins, GnRH analogs, & danazol have been shown to ↓ pain & ↑ time until recurrence (Fertil Steril 2008;90:S260; Hum Reprod 2011;26:3).

RECURRENT ABNORMAL UTERINE BLEEDING (AUB)

Definition and Etiology

AUB: Menstrual flow outside of nml vol, duration, regularity, or frequency. Excessive bld loss is based on pts’ perception.

Pathophysiology

• See PALM-COEIN table.

• Anovulation → no cyclic progesterone production → ↑ estrogen → ↑ endometrial proliferation → amenorrhea → eventually, endometrium overgrown & structurally fragile → random & dyssynchronous endometrial sloughing → irreg vaginal bleeding → AUB/menorrhagia. An anovulatory pt is always in follicular phase of ovarian cycle & in proliferative phase of endometrial cycle. No luteal or secretory phase b/c no cycles. Unopposed estrogen ↑ risk of endometrial hyperplasia.

Differential Diagnosis

• Always consider Preg or related complications (SAB, ectopic).

• Teens: MCC d/t persistent anovulation d/t immaturity or dysregulation of HPA (= nml physiology), coagulopathy, contraception, infxn, tumor.

• Reproductive age (19–39 y): Structural abnormalities (PALM), anovulatory cycles, contraception, endometrial hyperplasia. Cancer less common but may occur.

• Perimenopause: Endometrial hyperplasia, cancer, anovulatory bleeding d/t declining ovarian fxn (= nml physiology).

Diagnostic Workup (BMJ 2007;334:1110; Obstet Gynecol Clin N Am 2008;35:219)

• Detailed history & physical exam, including bimanual exam to evaluate uterus & speculum exam to evaluate cervix & vagina. Complete menstrual Hx is essent & can provide dx w/ suff confidence that rx can begin empirically.

• Regular, heavy menses usually anatomical lesion or bleeding d/o.

• Lab tests: Preg test, CBC, TSH. Consider pap smear & chlamydia testing. R/o bleeding disorders, particularly in teens. Serum progesterone in luteal phase >3 ng/mL sugg recent ovulation, but timing of test difficult w/ irreg menses.

• An EMB is not always req, except for >45 yo. Consider before rx if long-term unopposed estrogen exposure present, regardless of age.

• Imaging reserved to evaluate finding on physical, when sx persist despite rx, or suspicious for intrauterine pathology (AUB-P or AUB-L).

Treatment & Medications (Obstet Gynecol Clin N Am 2008;35:219; Menopause 2011;18:453)

• Treat underlying etiology. If no ↑ risk of endometrial hyperplasia, cancer, or underlying structural abnormalities, start empiric medical rx. Expect improv in 3 mo. Failure to improve → need to r/o other etiologies before changing mgmt. See also Chap. 2 for acute bleeding.

• Rx goals: (1) reverse abnormalities of endometrium d/t chronic anovulation, (2) induce or restore cyclic predictable menses of nml vol & duration.

• Surgical mgmt:

Acute surgical mgmt: Rare. If hemodynamic unstable, bleeding refrac to 2 doses of IV premarin, or bld loss that cannot be replaced w/ xfusion, OR mgmt (D&C) req. Should continue medical therapy after D&C. Informed consent should include hypogastric artery ligation & hysterectomy should D&C fail. Uterine artery embolization may be considered as an alternative, if available.

Endometrial ablation: High success rate. 25–50% are amenorrheic, & 80–90% have ↓ bleeding. Effective alternative to hysterectomy. ↑ success if pretreated w/ progest or GnRH. R/o cancer prior to Surg. Up to 1/3 will eventually elect for hysterectomy.

Hysterectomy: High satisfaction, but more morbidity & poor choice in pts w/ medical conditions w/ high risk for Surg.

POSTMENOPAUSAL BLEEDING

Definition, Epidemiology, & Etiology (Obstet Gynecol 2010;116:168)

• PMB: Vaginal bleeding occurring after ≥12 mo of amenorrhea

• PMB “is endometrial cancer until proven otherwise.” Malig w/ PMB = 1–14%. Predictive value depends on age & risks: Obesity, HTN, diabetes, low parity.

• Caused by cancer (10%), atrophy (60–80%), endometrial hyperplasia (2–12%), HRT (15–25%). Tamoxifen increases endometrial cancer risk. TVUS less useful d/t subepithelial stromal hypertrophy. Therefore any bleeding w/ tamoxifen → w/u.

Diagnostic Workup (Obstet Gynecol 2010;116:168)

• Comprehensive H&P: Pelvic exam to evaluate rectal, vulvar, vaginal, or cervical origin.

• Goal of endometrial eval: (1) exclude malig, (2) rx based on proper etiology (anatomic vs. nonatomic pathology)

• Endometrial eval:

Transvaginal US allows initial screening in some protocols. An EMS on TVUS <5 mm, has a risk of malig of 1:917. PPV 9% & NPV 99%. Sens 90%, spec 48% for endometrial cancer. About 50% of pts w/ initial TVUS → further eval (Obstet Gynecol 2009;113:462). Limitations: EMS not always visible, particularly w/ prior Surg, fibroids, obesity, adenomyosis. Incidental thick EMS in an asx pt does NOT require intervention. Often d/t polyps (82%) → no intervention b/c negligible risk that an asx polyp (ie, no bleeding) will harbor cancer (1:1000).

EMB: Accurate for excluding cancer, but only samples small focus of endometrium. Sens 99%, spec 98%. False negative ∼10%. High rate of insuff or failed sampling (0–54%) → further eval (Maturitas2011;68:155).

Sonohysterography: Imaging w/ saline infusion (SIS) overcomes some TVUS limitations.

3D US & Doppler adds no additional information at this time.

D&C: Useful when unable to obtain EMB (cervical stenosis, pt intolerance, etc.). Invasive: 1–2% complication rate. May miss 10% of endometrial lesions, & of these up to 80% are polyps.

Figure 5.3 Management of postmenopausal bleeding

DYSMENORRHEA

Definition & Epidemiology

• Dysmenorrhea = painful menstruation. One of the most common gyn complaints.

• Primary dysmenorrhea (PD) = Menstrual pain in the absence of underlying pathologic pelvic dz. Usually seen near time of menarche. Affects 43–91% of adols (depending on study criteria) (Contraception2010;81:185). PD ↓’s w/ ↑ age. Highest in 20–24 yo’s & ↓’s thereafter (Obstet Gynecol 2006;108:428).

• Secondary dysmenorrhea (SD) = Menstrual pain d/t pelvic condition or pathology. Risks: BMI <20, nulliparity, depression, premenstrual syn, sterilization, PID, h/o sexual assault, & heavy smoking.

Pathophysiology & Etiology

• PD d/t ↑ PGF2α in secretory endometrium → ↑ uterine contractility → painful menstrual cramps (Contraception 2010;81:185)

• SD most commonly d/t endometriosis, followed by adenomyosis, & IUD. Other causes:

Gyn etiology: Cervical stenosis (hematometria), PID, adhesive dz, fibroids, pelvic congestion, & congen malformations.

Nongynecologic etiology: Psychosomatic, IBS, inflamm bowel dz, UTI/dz, kidney stones, IC.

Clinical Manifestations & Diagnosis

• PD: Presents w/ or shortly after menarche. Midline, cramping pain, beginning w/ onset of menses. Pain worst 1st 24–36 h, c/w the highest levels of PG release. Resolves over 12–72 h (Contraception2010;81:185). Dx based on hx & nml pelvic exam. May be a/w HA, N/V, backache, & diarrhea. May occur as late as 1 y after menarche, but unlikely & should ↑ suspicion for SD.

• SD: Dx based on inconsistent hx & abn pelvic exam (eg, pelvic mass, abn vaginal discharge, pelvic tenderness not limited to time of menses). Consider SD if no resp to NSAIDs & OCPs, or if sx follow years of painless menses.

Treatment & Medications

• PD:

NSAIDs: 1st-line therapy. Works in ∼90% of pts. Start on day prior to menses, or at onset. If 1 NSAID is ineffective, switch to different class. Specific COX-2 inhibs (celecoxib) also shown to be effective.

OCP: Suppress ovulation & ↓ endometrial thickening → ↓ PG → ↓ pain. Low-dose OCs (20 mg ethinyl estradiol) can ↓ sx. Continuous OC (vs. monthly) will ↓ pain longer, but s/e extended regimen = breakthrough bleeding.

Depot medroxyprogesterone (150 mg IM q3mo): Not specifically studied in this pop. Presumed to ↓ endometrium thickness → ↓ PG → ↓ pain.

Levonorgestrel-releasing IUD: Profound local effect → suppression of endometrial growth → improv in sx.

Nifedipine (20–40 mg QD): Known effect on uterine contractility, but 1st-line therapy so effective that it is rarely req. S/e = flushing, tachy, & HAs.

Narcotics: Should be used as last-line therapy

Endometrial ablation: ↓ endometrium → ↓ sx. Not for those desiring fertility.

Nerve ablation: Observational studies support LUNA & presacral neurectomy to interrupt cervical pain fibers. Cochrane review sugg presacral neurectomy > LUNA > placebo/no rx. But insuff evid to recommend either (Obstet Gynecol 2006;108:428).

Figure 5.4 Management algorithm for dysmenorrhea

• SD:

NSAIDs & hormonal contraceptives are less likely be effective if SD present.

Mgmt of SD is rx of the underlying d/o.

PREMENSTRUAL DYSPHORIC DISORDER (PMDD) AND PREMENSTRUAL SYNDROME (PMS)

Definition and Epidemiology (Am J Psych 2012;169(5):465)

• PMS in about 30% regularly cycling . PMDD affects 3–8% of  w/ PMS.

• Classification of premenstrual disorders is based on gradation of premenstrual symptomatology: Mild (premenstrual sx) → mod PMS → sev PMDD

• Proposed DSM-V diagnostic criteria for PMDD: 5 or more of the following during the week prior to menses, declining w/i a few days after the onset of menses. At least 1 of the 5 sx must be a core symptom, representing 1 of the 1st 4 on the list.

Marked affective lability, irritability, or markedly depressed mood or marked anxiety; decreased interest in usual activities, difficulty in conc, lethargy, marked changes in appetite (overeating or food cravings), hypersomnia or insomnia, feeling overwhelmed, physical sx (breast tenderness, bloating, muscle or joint pain, or HA). Functional impairment in work, school, daily activities, & relationships.

Dx of exclusion (not exacerbation of another mood d/o like MDD, panic d/o, dysthymic d/o, personality d/o). Not attributed to a substance, medication or general medical condition.

Dx requires prospective documentation of sx for ≥2–3 menstrual cycles.

• Dx of PMS: Timing of sx occurs before menses & declines w/ the onset of menses. 1 or more of the following present, but no functional impairment:

Mild psychologic discomfort, bloating, wt gain, breast tenderness, periph swelling, aches/pains, ↓ conc, sleep disturbances, changes in appetite.

Etiology

• No specific mech identified. Variety of mood changes/destabilization involving serotonin, triggered by physiologic hormonal changes in susceptible individual.

Initial Workup

• Hx, physical, CMP, CBC, serum TSH. Menstrual hx w/ an eval of regularity of menstrual cycles; ovulation is req for dx.

• A 2–3-mo prospective menstrual calendar: Document sx & relationship to menses; sx ↑ at the time of ovulation & decline w/ onset of menses; a symptom-free week occurs during the follicular phase.

• DDx: Mood & personality disorders, domestic abuse, thyroid disorders, perimenopause, anemia, endometriosis, chronic fatigue syn, IBS, fibromyalgia

Treatment and Medications

• Goal to ↑ unaffected days & ↓ symptom severity → ↑ psychosocial functioning

No effective medical rx for PMS in empirical studies. High placebo resps (30–80%). Recommend: Support, lifestyle changes, diet, relaxation, exercise in mild–mod PMS. Limited/no efficacy: Vit B6 100 mg/d (max dose), Vit E 400 IU/d, calcium 600 mg BID (↓ 48% vs. 30% in placebo in PMS sx) & magnesium 200–360 mg/d.

• SSRIs are 1st-line rx for PMDD (meta-analysis of RCT demonstrated 60% resp rate) (Obstet Gynecol 2008;111(5):1181): Fluoxetine 20 mg/d, paroxetine 20–30 mg/d, citalopram 20–30 mg/d & sertraline 50–150 mg/d. Clomipramine & venlafaxine may be also be effective. Luteal phase only → smaller rx effect than daily dosing (Obstet Gynecol 2008;111(5):1175).

• Other rxs for PMDD:

Alprazolam 0.25 mg TID or QID prn. Use limited by dependence risk.

Medical oophorectomy w/ GnRH agonists: Leuprolide (add back therapy if rx is continued >3–6 mo) & danazol (limited use d/t s/e).

Surgical oophorectomy last form of permanent therapy when all other rxs have failed & trial of medical oophorectomy successful.

Less effective: Oral contraceptives w/ drospirenone & a 4-d pill-free interval, diuretic w/ spironolactone

CHRONIC PELVIC PAIN

Definitions and Etiology (Chapter 27. Chronic Pelvic Pain. Hopkins Manual of Gyn-OB, 4th ed. 2011)

• Noncyclic pain, at least 6 mo duration in the abdominal wall at or below the umbilicus or in the anatomic pelvis; causes functional disability or request for medical care.

• Pain is subjective & may or may not be a/w pelvic pathology or physical findings. Requires WIDE diff, possibly team eval/approach.

• Causes may be gastrointestinal (38%), urologic (31%), gyn (20%), musculoskeletal, neurologic, psychological (Br J Obstet Gyn 1999;106:1156)

Clinical Manifestations

• Gastrointestinal: Diarrhea, constip, flatulence, relationship of bowel mvmts w/ pain, hematochezia

• Urologic: Urgency, frequency, urinary incontinence, dysuria, nocturia, hematuria

• Gyn: Vaginal bleeding/discharge, dysmenorrhea, dyspareunia, infertility

• Neuropathic/musculoskeletal: Trauma, postural changes

Initial Workup

• Most common diagnoses: IBS (50–80%), IC (35–85%), endometriosis (33%), adhesions (24%), psychological or sexual abuse (40–50% prevalence).

• A detailed history & physical exam. Obtain pain hx, medical, surgical & gyn factors, pathology, operative reports, & prior pain evals

• Abdominal exam: Pain map, + Carnett’s sign (bilateral leg raise, or sit up; worsening pain consider musculoskeletal etiology as true visceral pain improves w/ tension of abdominal muscles.) Exam elements directed toward suspected cause.

• Lab: CBC, UA & cx, GC/CT, Preg test, wet prep, ESR

Diagnostic Workup/Studies

• If physical exam findings consistent w/ mass, TVUS to evaluate pelvic mass, hydrosalpinx. If abn→ consider MRI or CT.

• Diagnostic laparoscopy for endometrial implants w/ biopsies & histology (visual dx is correct only 10–90%)

• Validated questionnaire w/ the O’Leary-Sant Interstitial Cystitis Symptom Index: If score of ≥5 on screening (94% sens & 93% NPV) → cystoscopy + for glomerulations, ulcer (8%), ↓ bladder capacity → IC (Obstet Gynecol2002;100:337); validity of potassium intravesical sens test is uncertain (85% positive in CPP pts evaluated in general ob/gyn office).

• Colonoscopy as sx or exam indicate.

Treatment and Medications

• Multidisciplinary approach

• Empiric medical rx for the most likely cause. Endometriosis: NSAIDs, OCPs, medroxyprogesterone acetate 30–100 mg QD, danazol for 2–9 mo or Lupron 3.75 mg QMO. If no improv in 2–3 mo → invasive diagnostic testing. Chronic infectious etiology (∼18–35% of acute PID develop CPP, sterile pyuria in urethral syn), doxycycline 100 mg BID × 14 d. Manual therapy of myofascial pelvic trigger points – 65–70% improv (J Urol 2001;166:2226).

• Endometrial implants, windows, & endometriomas → excised & fulgurated; pain relief at 1 y in 45–85%; recurrence usually at 40–50 mo. Hysterectomy; no RCT (75% pain relief at 1-y f/u) (Obstet Gynecol 1995;86:941).

VESTIBULODYNIA

Definitions, Epidemiology, and Etiology (J Reprod Med 2004:49:772)

• Sev, localized pain of the vulva provoked by focal touch or pres, lasting >3 mo & not explained by another condition.

• 11–16% prevalence

• Unk cause. Current hypothesis: Insult to mucous membrane of the vulvar vestibule → chronic inflammation → central nervous system sensitization → allodynia. Risks include vulvovaginal candidiasis, OCP use, presence of IC.

Clinical Manifestations

• Cardinal sign: Sev pain upon vaginal penetration, touch or focal vulvar pres for 3–6 mo w/o relevant visible findings or clinically characterized neurologic d/o. Most common site of provoked pain → post fourchette.

• Provoked by coitus, vulvar contact w/ tampon, speculum, tight clothing, washing, or wiping vestibule; sitting, biking, or horseback riding.

Physical Exam and Diagnostic Workup

• Pelvic exam: Gross inspection, mapping by palpation w/ cotton tipped applicator to localize pain, single digit exam, speculum exam; tenderness in vulvar vestibule w/ or w/o areas of erythema; no pathognomonic features, no bx needed.

• A clinical dx of exclusion w/ history & physical exam

• Labs: Vaginal pH & microscopy, yeast culture

• R/o other causes: Infectious, inflamm, neoplastic, neurologic, musculoskeletal, psychosexual; depression, domestic abuse or relationship discord; DDx include fungal vulvitis, lichen planus, lichen sclerosus, lichen simplex chronicus, atopic or contact dermatitis, vulvar intraepithelial neoplasia

Subsequent Workup

• Treat vulvar dermatosis w/ steroids, if no improv in sx → poss LPV. Serial yeast cx if culture negative yet pt experiences recurrent vulvovaginal pruitus or burning.

Treatment and Medications

• Extensive pt education (www.nva.org) & vulvar care (unscented products, 5–10 min sitz baths)

• 1st-line therapy: Pelvic floor muscle rehabilitation w/ either topical gabapentin 6% or topical 5% lidocaine gel; 5 mL of topical lidocaine to the vestibule 20–30 min prior to vaginal intercourse

• Tricyclic antidepressants w/ nortriptyline or desipramine gradual max daily dose of 100–150 mg PO; alternative regimen w/ gabapentin (64% showed ↓ 80% of sx) (J Reprod Med 2007;52(2):103)

• Botulinum toxin type A injections

• Surgical intervention as a last rx (∼30–50%: Improv) Woodruff’s original perineoplasty, post, modified, or simplified vestibulectomy & vestibuloplasty.

FEMALE SEXUAL DYSFUNCTION

Definitions (DSM-IV-TR)

• 4 major categories of disorders characterized by recurrence or persistence of sx: Sexual desires, arousal, orgasmic, sexual pain. Each must be accompanied by distress or interpersonal difficulty.

• HSDD deficiency or lack of sexual thoughts, desire or receptivity. Sexual aversion d/o is an aversive resp to genital contact w/ a sexual partner.

• Sexual arousal d/o is inability to achieve sexual excitement subjectively or objectively.

• Sexual orgasmic d/o: Difficulty achieving orgasm w/ suff sexual arousal

• Sexual pain d/o: Dyspareunia or vaginismus & noncoital pain

Epidemiology

• 43% prevalence: Low sexual desire (22–39%); arousal problems (14–26%); orgasm (21%), sexual pain (7%) (JAMA 1999;281:537; Obstet Gyn 2008;112, 976)

Etiology

• Organic or psychological or a mix of both; more than 1 dysfxn may coexist. Risks: ↓ age, ↓ educational attainment, ↓ social status, urinary tract sx, sexual trauma

• Medical (depression, anxiety, urinary incontinence, ESRD, anemia, thyroid, DM, substance or EtOH abuse, cancers), meds (SSRIs – most commonly, beta-blockers, antipsychotics), current relationship, sociocultural factors, estrogen deficiency, abn gyn etiology

Pathophysiology

•  sexual resp cycle has 4 phases: Desire, plateau, orgasm, resolution as described by Masters & Johnson in 1966. Nonlinear model integrates emotional intimacy, sexual stimuli & relationship satisfaction; a sexual encounter may begin w/o desire initially present (Clin Update Women’s Health Care 2003;11(2):1).

Diagnostic Workup/Studies

• The Brief Sexual Symptom checklist, a screening questionnaire (J Sex Med 2010;337)

• Lab eval as clinically indicated: TSH, PRL, etc. H&P for most eval.

Treatment and Medications

• Nonpharmacologic therapy (1st line): Identify rx goals, treat reversible causes; psychoanalysis, sex therapy w/ requisite exercises (dilators, vibrators) & Eros Therapy (FDA approved), pelvic floor physical therapy, desensitization, Kegel, & relaxation exercises

• Pharmacologic therapy: For HSSD, non-FDA approved rx w/ 300-μg testosterone patch 2× weekly + ET for ≤6 mo; ET, a testosterone cream (0.5 g QD) topical (combined estrogen & testosterone therapy ↑ multi sexuality measures) (Menopause 2006;13:770).

• HRT for vasomotor & atrophy, low-dose vaginal postmenopausal ET for atrophy only; vaginal lubricants or moisturizers as an estrogen alternative; for dosing see Chap. on Menopause & therapy for urogenital atrophy.

MENOPAUSE

Definitions and Epidemiology (Fertil Steril 2012;97(4):843)

• Final menstrual period (FMP) defined by 12 mo of amenorrhea from a loss of ovarian activity. Perimenopausal transition: Wide fluctuation in hormonal profiles; ↑ irreg cycle length; quantitative FSH of >25 IU/mL on a random bld sample.

• FMP at <40 y = premature menopause (∼1%)

• Growing number of menopausal women. 37.9 million over 55 yo (2010) → 45.9 M (2020).

• Median age 51.4 y (Am J Epidemiol 2001;153:865). Gaussian distribution of 40–58 y.

• Leading cause of mortality is cardiovascular dz related (45%) > stroke > cancer.

Figure 5.5 Stages of reproductive aging

Etiology

• Reproductive axis is a negative neuroendocrine feedback loop. Reduced quality & quantity of aging follicles → ↓ inhibin & ↓ ovarian estrogen → ↑ FSH → accelerated loss of ovarian follicles → depleted ovarian follicle supply→ ovarian senescence

• α- & β-estrogen receptors are located throughout the body; ↓ estrogen → sx.

Clinical Manifestations

• Vasomotor instability: Hot flushes & night sweats (∼75%); most common during late menopausal transition (Stage –1) through early postmenopausal period (Stage +1). Self-limited w/ resolution in 1st 5 postmenopausal years; 25% symptomatic >5 y; high variability among individuals & cx.

• Urogenital atrophy: Pruritus, recurrent UTI, vaginal neuropathy in the distribution of pudendal nerve, sexual dysfxn, dyspareunia (up to 75%); most common during late postmenopause (Stage +2)

• Alterations in menstrual patterns: Chronic anovulation → heavy dysfunctional bleeding during late reproductive stage (Stage –3a) & menopausal transition (Stages –2, –1)

• Infertility secondary to oocyte depletion

• Increased cardiovascular dz risk: ↑ total cholesterol, ↑ markedly LDL-C.

• Accelerated bone loss: Spine bone density ↓ by 15–30% in 1st 5–7 postmenopausal years. Thereafter, it is 1–2% per year as compared to premenopausal bone loss rate of 13% per year. The effect is predominantly on trabecular bone (Hormone Therapy 2010;115(4):844).

• Decreased collagen support: ↓ skin collagen by 30% in 1st 5 years after menopause. There is an ∼2% ↓ per year for the 1st 10 y after established menopause.

• Increased endometrial & breast cancer risk d/t unopposed endogenous estrogen production

Physical Exam

• Habitus, race, serial ht. Pelvic exam: Vagina may appear thin, pale, dry, inflamed, lack rugae, petechial hemorrhages, cervical atrophy, narrowed or shortened vagina is a possibility; urethral caruncle may be present.

Diagnostic Workup/Studies

• Clinical dx from longitudinal assessment of absence of menses over 12 mo.

• Risk assessment for CVD (lifestyle, FHx, lipid profile) & osteoporosis. DEXA scan of the hip & vertebrae w/ resultant T-score (1–2% accuracy & precision). BMD may be used to diagnose osteoporosis, predict fracture risk & identify who would benefit from therapy. See Chap. 1 Osteoporosis.

Treatment and Medications

• Perimenopausal transition: Prolonged maximal physical energy, social & mental activities.

• VMSx classified mild (transient heat), mod (heat + sweating + permits continuation of activity), sev (heat + sweating + discontinuation of activity). Mod–sev VMSx = 7 hot flashes/d or 50–60 per week. HRT most effective for VMSx therapy (see section below).

• Mild urogenital atrophic sx, vaginal moisturizing agents on a regular basis before bedtime several times weekly & lubricants during intercourse, regular sexual activity.

• Urogenital atrophy: Systemic ET is the most effective for mod–sev sx; local vaginal Est Rx (rings, creams, tablets) w/ minimal systemic absorp & increased safety up to 1 y. Long-term effects lacking (Obstet Gynecol2010;115(4):843).

• Sexual dysfxn: Local estrogen for lubrication by increasing bld flow & sensation of vaginal tissues. Oral systemic ET is approved for rx of dyspareunia.

• Urinary sx: Vaginal ET Est Rx (in RCT ↓ risk of recurrent UTI) (Am J Obstet Gynecol 1999;180:1072)

• See Chap. 1 for osteoporosis mgmt.

• Primary & secondary prevention of CHD, stroke, VTE, osteoporosis. Recommend modifiable lifestyle change for primary & secondary prevention: Smoking cessation; control of HTN, dyslipidemia, & DM. Calcium suppl (1200–1500 mg daily), Vit D suppl (800 IU daily).

HORMONE THERAPY

Definitions

• HT comprises estrogen & progesterone therapy.

• ET comprises solely estrogen therapy.

• “Timing hypothesis” – timing of initiation of HT in relation to chronologic age/length of menopause affect risk of primary endpoints (Am J Epidemiol 2007;166;511); secondary analysis of WHI/observational studies → initiation of HT before 60 y of age or w/i 10 y of menopause may confer maximal cardioprotection for 6 or more years, improved QOL measures over 5–30 y (Climateric2012;15(3):217).

Indications

• Principal indication for HT is rx of VS. VS classified as mild, mod, or sev. FDA: Mod–sev VS is 8 hot flashes per day or 60 per week

• Use HT when benefits outweigh risks. Benefit:risk ratio changes w/ age & w/ onset of menopausally related sx (eg, VS, sleep disturbance, vaginal atrophy, dyspareunia, or diminished libido, affecting QOL).

• “Timing hypothesis” implies benefits of short-term HT use for VS outweigh CV risk when initiation of HT occurs in close proximity to onset of menopause in appropriately selected pts (Hormone Therapy2010;115(4):847).

Contraindications

• HT: H/o breast cancer, endometrial cancer, CHD, prev VTE or CVA, active liver dz, or high risk for these complications.

Physical Exam

• Estrogen deficiency → thin, pale vaginal mucosa, loss of elasticity & rugal folds, diminished secretions, shortened or narrowed vagina, moisture content ↓, the pH ↑ (usually >5), & mucosal inflammation & petechiae.

Assessment of the Risk–Benefit Ratio

• Women enrolled in WHI, a RCT w/ primary CV event had a mean age of 63–64 y & >10 postmenopausal years.

• In a secondary analysis of WHI data ET arm, statistically signif reduction in CV endpoints (MI, coronary artery revascularization, & coronary death) in those aged 50–59.

Treatment and Medications

• HT: Systemic ET is most effective rx for mod–sev VS; only therapy approved by the FDA for this indication (↓ 75% symptom).

• HT should be guided by use of smallest doses & shortest duration for symptomatic relief.

• Nonhormonal therapy as alternative in noncandidates for HT & mild VS: Lifestyle changes (reduction in body temperature, healthy wt maint, smoking cessation, relaxation techniques, acupuncture)

• Meds acting on central neurotransmitter pathways, decreasing central noradrenergic tone: Clonidine 0.1 mg weekly transdermal patch, (mainstay of nonhormonal therapy, but not FDA approved) paroxetine 10–20 mg/d or controlled release 12.5–25 mg/d, venlafaxine extended release 37.5–75 mg/d, gabapentin 300 mg/d to 300 mg TID.

• Duration of rx: Short-term therapy goal (≤2–3 y) is symptomatic relief; annual reassessment of HT need.

• Discontinuation of rx: Abrupt withdrawal of exogenous estrogen → return of hot flashes & other sx. Based on WHI, ∼55% recurrence w/ abrupt cessation. Estrogen taper is not more effective than abrupt cessation. Limited trial data; if recurrent hot flashes w/ no resolution→ nonhormonal medication. If ineffective, restart estrogen at the lowest dose poss (risk:benefit ratio) w/ plan to attempt discontinuation in the prox future.

• QOL: Whether HT improves HQOL is unk; data not available of effect of HT on global QOL (the sense of well-being w/ or w/o sx or physical impairments).

PREGNANCY TERMINATION

Early Medical Termination

• Utilizes an established medical regimen to induce an abortion up to 63 d of EGA; A failed medical abortion is defined as the presence of a gestational cardiac activity on transvaginal USG 2 w following medical abortion.

• 6% of all abortions in US are medical; <1% of medical terminations <49 d fail, <1% require surgical intervention by D&C for hemorrhage

Medical Terminations in the Second Trimester or Termination by Induction

• Upper limit for 2nd trimester surgical termination varies by state.

• Induction abortion is the termination of Preg by stimulation of labor-like contractions that cause eventual expulsion of the fetus & placenta from the uterus.

• US physicians must comply w/ the federal Partial-Birth Abortion ban Act of 2003, which bans abortions wherein the physician deliberately delivers a living fetus vaginally, the point at which any part of the fetal trunk above the navel is outside the woman’s body, & after the fetus reaches the specified point in either presentation breech or vertex, the physician performs an overt & separate maneuver from deliv to kill the fetus.

• 10–15% occur in the 2nd trimester; ≥13 EGA (12%); 16–20 EGA (3.8%); >21 EGA (1.4%) (MMWR Surveill Summ 2008;57:SS–13)

• Mifepristone & misoprostol (mean 6–11 h for completion). Alternatively, prostaglandin E1 when mifepristone is not available (mean 9–20 h for completion).

Surgical Terminations

• Univ periabortal antibiotic ppx is effective & inexpensive (↓ 42% decreased risk of postabortal infxn): Doxycycline 100 mg PO 1 h preoperatively & a single 200 mg PO dose postprocedure.

• Unsensitized Rh(D) women should receive Rh(D) Ig w/i 72 h postabortion. 50 μg dose at <13 wga & 300 μg dose <13 wga.

• Contraceptive care initiation w/ long-acting reversible contraceptives may ↑ contraceptive use, improve continuation, reduce rpt Preg & rpt abortion.

• Potential complications may be immediate (intraoperatively or in recovery room) or delayed (w/i few hours postprocedure to 2 w): Retained products of conception, hemorrhage, uterine injury: Cervical tears, uterine perforation, syncope, thromboembolic & cardiorespiratory disorders. Delayed complications also include infxn, persistent intrauterine or ectopic Preg.

• D&C: Most commonly performed for 7–13 w EGA. By convention D&C = <14 w.

Manual vacuum aspiration – use at <10 w EGA, 60 mm Hg suction

Electric vacuum aspiration – for all GAs, 60 mm Hg suction

• D&E: By convention, D&E = >14 w EGA.

Mechanically dilate uterine cervix, permitting evacuation of fetal & placental tissue.

Most common technique for 2nd trimester terminations (>96%)