Reproductive Endocrinology

01 Reproductive Physiology — HPG Axis & the Menstrual Cycle

Reproductive endocrinology and infertility (REI) is the subspecialty of obstetrics and gynecology that manages disorders of the reproductive hormonal axis, infertility, and assisted reproductive technology (ART). An REI scribe must understand the hypothalamic-pituitary-gonadal (HPG) axis because every diagnosis, medication, and stimulation protocol manipulates some node of this pathway.

The HPG Axis

The hypothalamus secretes gonadotropin-releasing hormone (GnRH) in a pulsatile fashion into the hypophyseal portal circulation. GnRH stimulates the anterior pituitary to release two gonadotropins: follicle-stimulating hormone (FSH) and luteinizing hormone (LH). In females, FSH drives recruitment and growth of ovarian follicles and stimulates granulosa cells to produce estradiol via aromatization of androgens. LH stimulates theca cells to produce androgens (the substrate for aromatization) and, at mid-cycle, triggers ovulation. In males, FSH supports Sertoli cells and spermatogenesis, while LH stimulates Leydig cells to produce testosterone.

Feedback is tightly regulated. Estradiol and progesterone exert negative feedback on GnRH and FSH/LH throughout most of the cycle, but late-follicular-phase estradiol (rising above ~200 pg/mL sustained for ~48 hours) flips to positive feedback, triggering the LH surge. Inhibin B (granulosa cell product in the follicular phase) and inhibin A (corpus luteum product in the luteal phase) selectively suppress FSH.

The Menstrual Cycle

An idealized cycle is 28 days long, but anything between 21 and 35 days with cycle-to-cycle variation under 7 days is considered ovulatory. The cycle has two hormonally defined phases separated by ovulation:

Follicular phase (days 1–14): Menstruation begins on day 1. Low estradiol and progesterone allow FSH to rise, recruiting a cohort of antral follicles. A single dominant follicle (typically the most FSH-sensitive) is selected around day 5–7 and produces rising estradiol. The endometrium is in the proliferative phase — estradiol-driven glandular and stromal growth. When estradiol peaks (~200–300 pg/mL from a mature follicle 18–22 mm), the LH surge fires and ovulation occurs ~36 hours later.

Luteal phase (days 14–28): The ruptured follicle becomes the corpus luteum, producing progesterone (and continued estradiol). The endometrium enters the secretory phase — tortuous glands, stromal edema, and a receptive implantation window (~days 20–24). If no pregnancy occurs, the corpus luteum involutes, progesterone drops, and menstruation begins. If implantation occurs, the embryo secretes hCG, rescuing the corpus luteum until placental steroidogenesis takes over at ~7–9 weeks (luteal-placental shift).

Female Reproductive Anatomy

The female reproductive tract consists of the ovaries, fallopian tubes (with fimbriated ends, ampullary segment where fertilization occurs, and interstitial segment passing through the uterine wall), uterus (fundus, body, lower uterine segment, cervix), and vagina. Each ovary is anchored by the ovarian ligament, suspensory ligament of the ovary (containing the ovarian vessels), and mesovarium. Knowing these relationships matters when interpreting imaging and dictation from egg retrievals, laparoscopies, and HSG reports.

02 Scribe Documentation Framework in REI

REI notes blend an OB/GYN-style gynecologic history with a fertility-specific narrative. A new consult can easily take 45 minutes and generates a dense multi-page note. Follow-ups during active ART cycles are short, number-heavy, and follow a repeating template.

03 The Infertility Workup — Female & Male Evaluation

The standard infertility workup evaluates four functional domains: ovulation, ovarian reserve, tubal patency, and sperm. Uterine cavity evaluation is added when indicated. ASRM Practice Committee: Fertility evaluation of infertile women (2021) defines the baseline evaluation.

04 Ovulatory & Anovulatory Disorders Endocrine

Anovulation and oligo-ovulation account for roughly 25% of female infertility. The WHO classification, adopted by REI practice, divides anovulation into three groups:

A separate WHO category (sometimes called Group IV) is hyperprolactinemic anovulation, covered in its own section below. Management of anovulation depends on the category: WHO II responds to ovulation induction with letrozole or clomiphene; WHO I requires exogenous gonadotropins or pulsatile GnRH; WHO III generally requires donor egg or aggressive IVF with poor prognosis.

05 Polycystic Ovary Syndrome (PCOS) Endocrine

PCOS is the most common endocrine disorder in reproductive-age women (8–13% prevalence) and the single most common cause of anovulatory infertility. It is a syndrome — meaning it is diagnosed by a constellation of features rather than a single test.

Pathophysiology

PCOS is driven by a combination of increased GnRH pulse frequency (favoring LH over FSH), ovarian and adrenal hyperandrogenism, and peripheral insulin resistance. Elevated LH stimulates theca cell androgen production; relative FSH insufficiency impairs aromatization and follicular maturation, leaving many small antral follicles arrested at ~5–8 mm — the classic polycystic ovarian morphology. Insulin resistance amplifies ovarian androgen production and reduces SHBG, raising free testosterone.

Diagnosis: Rotterdam Criteria

The Rotterdam criteria (2003), reaffirmed by the 2023 International PCOS Guideline, require 2 of 3 of the following after exclusion of other causes (thyroid disease, hyperprolactinemia, non-classical CAH, Cushing, androgen-secreting tumor):

Clinical Presentation & Workup

Patients present with oligomenorrhea/amenorrhea, infertility, hirsutism, acne, obesity, and acanthosis nigricans. Long-term risks include endometrial hyperplasia and carcinoma (from unopposed estrogen), type 2 diabetes, metabolic syndrome, NAFLD, obstructive sleep apnea, and cardiovascular disease. Workup includes total testosterone, DHEA-S, 17-OH progesterone (to rule out non-classical CAH), TSH, prolactin, 2-hour OGTT or HbA1c, lipid panel, and pelvic ultrasound.

Management

Non-fertility: Lifestyle modification (first-line; even 5–10% weight loss restores ovulation in many), combined oral contraceptives for cycle regulation and androgen symptoms, metformin for insulin resistance and metabolic risk, spironolactone for hirsutism, endometrial protection with progestin.

Fertility: Letrozole is first-line ovulation induction (PPCOS II trial) — superior live-birth rate compared to clomiphene in PCOS. Second-line: gonadotropins, laparoscopic ovarian drilling. Third-line: IVF (with attention to OHSS risk — PCOS patients are high responders).

06 Diminished Ovarian Reserve & Premature Ovarian Insufficiency Endocrine

Diminished ovarian reserve (DOR) describes a quantitative and/or qualitative reduction in the remaining oocyte pool for age. It is not a disease per se but a prognostic finding associated with reduced response to stimulation and lower cycle success rates. ASRM: Testing and interpreting measures of ovarian reserve (2020) is the reference.

Premature Ovarian Insufficiency (POI)

POI, formerly "premature ovarian failure," is defined as hypergonadotropic hypoestrogenic ovarian dysfunction in women younger than 40, with amenorrhea (or markedly oligomenorrhea) for at least 4 months and two FSH levels > 25–40 IU/L at least one month apart. Etiologies include idiopathic, genetic (Turner 45,X mosaicism, fragile X premutation FMR1), autoimmune (oophoritis, polyglandular syndromes), iatrogenic (chemotherapy, pelvic radiation, bilateral oophorectomy), and infectious. Workup includes karyotype, FMR1, adrenal autoantibodies, TSH, and thyroid autoantibodies. Management emphasizes hormone replacement therapy until natural menopause age (~51), bone health, cardiovascular risk management, and — for fertility — donor egg IVF. Spontaneous pregnancies occur in ~5–10% and cannot be reliably induced.

07 Hypogonadotropic Hypogonadism & Hypothalamic Amenorrhea Endocrine

Hypogonadotropic hypogonadism is the hypothalamic or pituitary failure to stimulate the ovaries — low FSH, low LH, low estradiol. The most common REI presentation is functional hypothalamic amenorrhea (FHA) from low body weight, excessive exercise, or chronic stress. Other etiologies include Kallmann syndrome (congenital GnRH deficiency with anosmia), pituitary adenomas, Sheehan syndrome, infiltrative disease (sarcoid, hemochromatosis), and prior cranial irradiation.

Workup includes FSH/LH/estradiol, prolactin, TSH, pituitary MRI if central cause suspected, and assessment of energy availability. Endocrine Society guideline on FHA (2017) emphasizes restoration of energy balance (nutrition, reduced exercise, psychological support) as first-line management. For fertility, pulsatile GnRH (where available) or exogenous gonadotropins (FSH plus LH activity) induce ovulation. Clomiphene does not work in FHA because there is no estrogen-driven feedback to block.

08 Hyperprolactinemia & Pituitary Disorders Endocrine

Prolactin suppresses GnRH pulsatility, producing oligomenorrhea/amenorrhea, anovulation, galactorrhea, and infertility. Causes include pregnancy (always exclude first), medications (antipsychotics, metoclopramide, SSRIs, methyldopa, verapamil), hypothyroidism (TRH stimulates prolactin), prolactinoma (microadenoma < 10 mm, macroadenoma ≥ 10 mm), stalk effect from a non-prolactin-secreting sellar mass, chronic kidney disease, and stress/recent breast exam.

Evaluation: repeat prolactin fasting and without recent breast/nipple stimulation, TSH, pregnancy test, pituitary MRI if persistent elevation or very high levels (> 100 ng/mL usually indicates adenoma). Management is dopamine agonist therapy — cabergoline (first line, 0.25–0.5 mg twice weekly) is preferred over bromocriptine for efficacy and tolerability. Most micro- and macroadenomas shrink substantially on cabergoline, and ovulation/fertility often return within weeks to months. Endocrine Society hyperprolactinemia guideline (2011).

09 Endometriosis & Adenomyosis Pelvic

Endometriosis is the presence of endometrial-like glands and stroma outside the uterine cavity, most commonly on the peritoneum, ovaries (endometriomas / "chocolate cysts"), pelvic ligaments, and bowel/bladder serosa. It affects 6–10% of reproductive-age women and up to 30–50% of women with infertility. It contributes to infertility via distorted pelvic anatomy, adhesions, impaired folliculogenesis, altered peritoneal environment, and reduced implantation.

Clinical Presentation & Diagnosis

Cyclic pelvic pain, dysmenorrhea, dyspareunia (especially deep), dyschezia, infertility, abnormal bleeding. Physical exam may reveal uterosacral nodularity, fixed retroverted uterus, adnexal tenderness. TVUS identifies endometriomas; MRI characterizes deep infiltrating endometriosis. Definitive diagnosis is histologic from laparoscopic biopsy, though empiric diagnosis and treatment are now common. ESHRE Endometriosis Guideline (2022) supports clinical and imaging diagnosis without mandatory laparoscopy.

ASRM (rASRM) Staging

Management

For pain: NSAIDs, combined oral contraceptives, progestins (norethindrone acetate, dienogest), GnRH agonists (leuprolide) with add-back therapy, GnRH antagonists (elagolix, relugolix), and laparoscopic excision or ablation. For fertility: expectant management in mild disease, surgical excision may improve spontaneous conception in early stages, IVF for moderate-severe disease or failed other therapies. Endometrioma resection is weighed carefully because cystectomy can further reduce ovarian reserve.

Adenomyosis

Ectopic endometrial glands within the myometrium, causing a bulky globular uterus, heavy menstrual bleeding, dysmenorrhea, and reduced implantation/pregnancy rates. Imaging features on TVUS and MRI include a thickened junctional zone (> 12 mm on MRI), myometrial cysts, and asymmetric myometrial thickening. Management mirrors endometriosis; definitive cure is hysterectomy (not fertility-compatible).

10 Uterine Fibroids, Polyps & Intrauterine Adhesions Uterine

Uterine Fibroids (Leiomyomas)

Benign smooth-muscle tumors of the uterus, extremely common (up to 70% lifetime prevalence). Classified by location — submucosal (protruding into the cavity, highest fertility impact), intramural, and subserosal. The FIGO leiomyoma classification (0–8) subdivides these further, with Types 0–2 being submucosal:

Submucosal and cavity-distorting intramural fibroids reduce implantation and increase miscarriage. Management for fertility includes hysteroscopic myomectomy (Types 0–2), abdominal or laparoscopic/robotic myomectomy (Types 3–4 large), and expectant management for small non-cavity-distorting fibroids. ASRM: Removal of myomas in asymptomatic patients (2017).

Endometrial Polyps

Benign focal overgrowths of endometrial glands and stroma projecting into the cavity. Associated with abnormal uterine bleeding and reduced implantation. Diagnosed by SIS or hysteroscopy; removal by hysteroscopic polypectomy before IVF is routine.

Asherman Syndrome / Intrauterine Adhesions

Scarring within the uterine cavity, most often following aggressive D&C (especially after retained products of conception or postpartum). Presents with hypomenorrhea, amenorrhea, cyclic pain, recurrent loss, or infertility. Diagnosed by hysteroscopy (gold standard), SIS, or HSG. Treatment is hysteroscopic adhesiolysis followed by estrogen therapy and adhesion prevention strategies (balloon stent, gel, IUD). Prognosis depends on severity per the ESGE classification.

11 Tubal Factor, Hydrosalpinx & Congenital Uterine Anomalies Anatomic

Tubal Factor Infertility

Accounts for ~25–35% of female infertility. Causes include prior pelvic inflammatory disease (chlamydia, gonorrhea), tubal surgery, prior ectopic pregnancy, endometriosis, tuberculosis, and prior tubal ligation. Diagnosis is by hysterosalpingogram (HSG) — bilateral free spill indicates patent tubes; unilateral or bilateral blockage, hydrosalpinx, or cornual occlusion is documented.

Hydrosalpinx

A fluid-filled obstructed fallopian tube, visible as a tubular cystic adnexal structure on ultrasound. Hydrosalpinx fluid is embryotoxic and halves IVF implantation/live birth. ASRM: Role of tubal surgery in the era of ART (2021) recommends salpingectomy or proximal tubal occlusion before IVF for any ultrasound-visible hydrosalpinx.

Congenital Uterine (Müllerian) Anomalies

Abnormal fusion of the paired paramesonephric (Müllerian) ducts during embryogenesis. The ASRM/ESHRE classification includes:

3D ultrasound and MRI distinguish septate from bicornuate uteri — the distinction is critical because septate is corrected hysteroscopically, while bicornuate requires abdominal metroplasty (rarely done).

12 Male Factor Infertility Male

Male factor contributes to ~40–50% of infertility (as sole or contributing factor). The semen analysis is the cornerstone of evaluation. WHO 2021 (6th edition) reference lower limits define the common abnormalities:

Terminology

Oligospermia — low sperm count; asthenospermia — poor motility; teratospermia — abnormal morphology; oligoasthenoteratospermia (OAT) — all three; azoospermia — no sperm in ejaculate; aspermia — no ejaculate (retrograde ejaculation, obstruction).

Azoospermia — Obstructive vs Non-Obstructive

Obstructive (OA): Normal testicular volume, normal FSH, normal testosterone. Causes: CBAVD (cystic fibrosis), post-infectious, iatrogenic (vasectomy, hernia repair). Sperm can usually be retrieved surgically (PESA, MESA, TESA). Non-obstructive (NOA): Small testes, elevated FSH, variable testosterone. Causes: Klinefelter 47,XXY, Y-chromosome microdeletion (AZFa/b/c), cryptorchidism, chemotherapy/radiation, Sertoli-cell-only syndrome. Sperm retrieval requires microdissection TESE with variable success (30–60%).

Varicocele

Dilated pampiniform plexus veins, usually left-sided (90%). Associated with abnormal semen parameters via testicular hyperthermia and oxidative stress. Graded by palpation: Grade 1 palpable only with Valsalva, Grade 2 palpable at rest, Grade 3 visible through scrotal skin. Varicocelectomy is offered to men with palpable varicocele, abnormal semen, and otherwise unexplained infertility per AUA/ASRM Male Infertility Guideline (2021).

Male Hypogonadism & Exogenous Testosterone

Exogenous testosterone suppresses pituitary LH/FSH and shuts down spermatogenesis — a common, underrecognized cause of secondary male infertility. Management: stop testosterone, treat with clomiphene, hCG, and/or hMG to restore intratesticular testosterone and spermatogenesis. This often takes 6–18 months. Sperm DNA fragmentation testing may be ordered for unexplained infertility, recurrent IVF failure, or RPL.

13 Recurrent Pregnancy Loss (RPL) Loss

ASRM defines recurrent pregnancy loss as two or more failed clinical pregnancies documented by ultrasound or histology (ESHRE definition allows biochemical losses). Only ~50% of RPL workups identify a definitive cause. ASRM Practice Committee: Evaluation of RPL (2012) and ESHRE RPL Guideline (2018).

Management

Targeted based on identified cause: hysteroscopic septoplasty, progesterone supplementation (controversial, most benefit in women with 3+ prior losses), levothyroxine for hypothyroidism, anticoagulation (low-dose aspirin + LMWH) for confirmed antiphospholipid syndrome, IVF with PGT-SR for balanced translocation carriers, IVF with PGT-A considered in recurrent aneuploid losses. MTHFR genotyping is NOT recommended — it is not an established RPL cause despite historical testing. Empiric treatments (IVIG, intralipid, lymphocyte immunotherapy) are not evidence-based and generally discouraged.

14 Unexplained & Secondary Infertility Evaluation

Unexplained infertility is a diagnosis of exclusion — ovulatory cycles, normal semen analysis, patent tubes, and a normal uterine cavity after a complete workup. It accounts for ~15–30% of couples. Management ladder: expectant management (younger women), ovulation induction with timed intercourse, OI plus IUI, and IVF. ASRM: Evidence-based treatments for couples with unexplained infertility (2020).

Secondary infertility is inability to conceive after a prior successful pregnancy. The workup is identical to primary infertility; age-related decline in ovarian reserve and interval-acquired issues (new male factor, tubal disease, retained products or adhesions from a prior delivery) are common.

15 Fertility Preservation & Oncofertility Preservation

Fertility preservation covers patients facing gonadotoxic therapy (chemotherapy, pelvic radiation, bilateral oophorectomy or orchiectomy), those with a gender identity transition plan, and those pursuing elective ("social") preservation. ASCO Fertility Preservation Guideline update (2018) is the standard oncology-facing reference.

Random-start protocols (stimulation begun in the luteal phase rather than waiting for the next menses) are commonly used in oncofertility to minimize delay to chemotherapy. Letrozole co-administration is used for hormone-sensitive cancers (e.g., breast cancer) to keep peak estradiol lower during stim.

16 Third-Party Reproduction & Donor Gametes Third-Party

Third-party reproduction involves donor eggs, donor sperm, donor embryos, or a gestational carrier. REI clinics perform extensive screening, counseling, and psychological evaluation before these cycles.

Donor egg IVF: Indicated for POI, severe DOR, prior poor IVF response, genetic disease, or advanced maternal age. Donors are screened for medical history, genetic carrier status, infectious disease (per FDA 21 CFR 1271), and undergo psychological evaluation. Cycles can be fresh (synchronized with recipient endometrial prep) or frozen donor egg bank cycles.

Donor sperm: Used for azoospermia without viable retrieval, severe genetic disease, single women by choice, and same-sex female couples. All donor sperm is quarantined for 6 months with repeat infectious disease testing per FDA.

Gestational carrier (GC): A woman who carries a pregnancy conceived from intended parents' (or donors') gametes via embryo transfer. Distinct from traditional surrogacy (which uses the carrier's own egg and is rarely performed today). Indicated for absolute uterine factor (MRKH, hysterectomy, severe Asherman), medical contraindication to pregnancy, or same-sex male couples. Legal contracts are mandatory and state laws vary widely. ASRM guidance on gestational carriers (2022).

17 Assisted Reproductive Technology (ART) Procedures Procedure

Ovulation Induction (OI)

Letrozole (Femara) 2.5–7.5 mg days 3–7 — an aromatase inhibitor; first-line in PCOS and unexplained infertility per PPCOS II. Clomiphene (Clomid) 50–150 mg days 3–7 or 5–9 — a SERM blocking hypothalamic estrogen feedback, raising endogenous FSH. Both typically produce 1–2 mature follicles. Cycles are monitored with follicle tracking ultrasound and timed intercourse or IUI. Expect the REI doctor to order CD3 baseline, mid-cycle monitoring, and trigger hCG 36 hours before ovulation/insemination.

Intrauterine Insemination (IUI)

Washed, concentrated sperm is placed directly into the uterine cavity using a soft catheter at the time of ovulation. Indicated for mild male factor, cervical factor, unexplained infertility, same-sex couples, and donor sperm cycles. Typically combined with OI. Success rates of 8–15% per cycle depending on age and diagnosis.

Controlled Ovarian Stimulation (COS) for IVF

Exogenous gonadotropins recruit and grow multiple follicles to maturity, overriding normal cohort selection. Two dominant protocols:

Egg Retrieval (Oocyte Pickup, OPU)

Transvaginal ultrasound-guided needle aspiration of follicles under IV sedation, typically 10–20 minutes. Each follicle is aspirated and flushed; follicular fluid is handed to embryology to identify cumulus-oocyte complexes. Number and maturity (MII, MI, GV) are documented. Risks include bleeding, infection, anesthesia, damage to adjacent structures, and OHSS.

Fertilization — Conventional IVF vs ICSI

Conventional insemination: ~100,000 motile sperm are placed in the dish with each oocyte. Intracytoplasmic sperm injection (ICSI): A single sperm is microinjected into each mature (MII) oocyte. Indications: severe male factor, prior fertilization failure, surgically retrieved sperm, PGT cycles (to avoid paternal DNA contamination). Fertilization is assessed at ~16–18 hours for pronuclei.

Embryo Culture & Transfer

Embryos are cultured to cleavage stage (day 3, ~8 cells) or blastocyst stage (day 5–6). Blastocyst culture allows better selection and is the norm in most US programs. Fresh embryo transfer — transfer during the same cycle as retrieval. Frozen embryo transfer (FET) — embryos are vitrified and transferred in a subsequent programmed or natural cycle. FET has become more common because it allows PGT, avoids OHSS, and may improve outcomes in certain populations. Endometrial preparation for programmed FET: estradiol (oral, transdermal, or vaginal) for ~2 weeks to build lining, then progesterone (IM, vaginal, or combined) to create the implantation window, with transfer on progesterone day 5 (blastocyst) or day 3 (cleavage).

Preimplantation Genetic Testing (PGT)

Performed on a trophectoderm biopsy of blastocyst-stage embryos, with embryos frozen awaiting results.

• PGT-A (aneuploidy): Screens for chromosomal abnormalities. Improves per-transfer success and may reduce miscarriage; does not improve cumulative live birth in the general population and is controversial in younger patients.
• PGT-M (monogenic): Tests for specific single-gene disorders (cystic fibrosis, sickle cell, Huntington, BRCA, fragile X, etc.) — requires custom probe development.
• PGT-SR (structural rearrangement): For carriers of balanced translocations and inversions.

Mosaic embryos (mixed euploid/aneuploid cell lines on biopsy) are a distinct result category; low-level mosaic embryos may be transferred with appropriate counseling and have produced healthy live births.

Surgical Sperm Retrieval

PESA — Percutaneous epididymal sperm aspiration. MESA — Microsurgical epididymal sperm aspiration (open, microscope-assisted). TESA — Testicular sperm aspiration (needle). TESE / micro-TESE — Testicular sperm extraction (open biopsy; microdissection variant for non-obstructive azoospermia). Sperm retrieved is typically used with ICSI.

Diagnostic & Office Procedures

Hysterosalpingogram (HSG): Fluoroscopic study where iodinated contrast is injected through the cervix to outline the cavity and tubes. Performed in follicular phase after menses, before ovulation. Reports comment on cavity contour, tubal fill, free spill, loculation, and any hydrosalpinx.

Saline infusion sonogram (SIS) / sonohysterogram: Transvaginal ultrasound with saline infusion to distend the cavity and detect polyps, submucosal fibroids, and adhesions.

Hysteroscopy: Direct visualization of the cavity with a thin scope; used diagnostically and for operative procedures (polypectomy, myomectomy, septoplasty, adhesiolysis).

Laparoscopy: Minimally invasive surgical exploration, used for endometriosis diagnosis/treatment, salpingectomy, tubal reconstruction, and ovarian cystectomy.

Endometrial biopsy: Office sampling for histologic dating, hyperplasia screening, or chronic endometritis (CD138 staining).

18 OHSS & Other ART Complications Complication

Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication of ovarian stimulation driven by VEGF-mediated capillary leak in hCG-exposed, hyperstimulated ovaries. Presents 3–10 days after trigger (early) or after pregnancy establishes (late). High-risk features: PCOS, high AMH (> 3.5), high AFC, prior OHSS, peak estradiol > 3500–5000, > 20 follicles on stim ultrasound.

ASRM: Prevention and treatment of OHSS (2016) emphasizes prevention: antagonist protocols, agonist triggers in high responders, freeze-all cycles, cabergoline prophylaxis, and individualized gonadotropin dosing. Management: supportive care with fluids, analgesia, VTE prophylaxis, paracentesis for tense ascites, and admission for severe disease.

Other Complications

Multiple gestation: Historic main risk of IVF; now mitigated by elective single embryo transfer (eSET). Ectopic pregnancy: ~2–4% after IVF (higher in tubal factor). Bleeding, infection, injury at retrieval. Anesthesia complications. Implantation failure and repeat IVF failure trigger further workup: repeat cavity evaluation, endometrial biopsy for chronic endometritis, thyroid and prolactin, PGT-A consideration, sperm DNA fragmentation, immunologic evaluation in select cases.

19 Imaging, Labs & Diagnostics Diagnostics

Transvaginal Ultrasound (TVUS)

The workhorse of REI. Used for baseline ovarian and uterine assessment, AFC, follicle tracking during stim, endometrial measurement, cyst characterization, and embryo transfer guidance. You will document: ovarian volumes, follicle number by size, endometrial thickness (mm) and pattern (trilaminar/triple-stripe, homogeneous, hyperechoic), and any abnormalities (cysts, fibroids, polyps, hydrosalpinx, free fluid).

Key Lab Values

20 Medications You Must Know Meds

21 Classification Systems & Criteria Reference

Most classifications referenced in REI notes are already enumerated above in their condition sections — Rotterdam (PCOS), rASRM (endometriosis), FIGO (fibroids), WHO (anovulation), ASRM (Müllerian), WHO 2021 (semen), OHSS severity. Two more are worth memorizing:

22 Physical Exam & Pelvic Exam in REI

The REI physical exam is focused and targeted. Full exams happen at the new consult; subsequent monitoring visits are usually a TVUS only.

On pelvic ultrasound you will write: "Uterus anteverted, normal contour, [X.X] cm. Endometrial stripe [X] mm, [pattern]. Right ovary [volume], [N] antral follicles, [dominant follicle sizes]. Left ovary [volume], [N] antral follicles, [dominant follicle sizes]. No hydrosalpinx. No free fluid." This template repeats across every monitoring visit.

23 Abbreviations Master List

Cycle & Physiology

Diagnoses

Procedures & ART

Medications

24 Sample HPI Templates

These templates reflect the typical rhythm, content, and terminology of an REI clinic note. Use them as scaffolds.

25 References & Sources

Clinical Practice Guidelines

Landmark Clinical Trials

Diagram & Figure Sources