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OG28.1-4,OG30.1-2 | Infertility and Endocrine Gynaecology — PBL Case

CLINICAL SETTING

Dr Preethi, a resident in the gynaecology outpatient clinic at a tertiary care centre, sees her first infertility couple of the morning. Meena, a 31-year-old school teacher, and her husband Rajan, a 33-year-old software engineer, have been trying to conceive for 22 months. They were married 2.5 years ago. Meena's menstrual cycles are irregular — she has 6–7 periods per year, with intervals ranging from 35 to 90 days. She reports mild acne on her jaw and chin that has been present since her late teens. She had moderate weight gain (8 kg) over the past 3 years and her current BMI is 31. There is no dysmenorrhoea, no pelvic pain, no galactorrhoea, and no history of previous pelvic surgery or pelvic inflammatory disease. She is not on any medications. Rajan has no prior medical history and has never had a fertility assessment. The couple is visibly anxious. Meena says: 'We have been waiting a long time. We were hoping it would happen on its own. We are worried now.' Dr Preethi begins her systematic workup.

Trigger 1: Initial History and Examination — Setting the Framework

Dr Preethi completes her clinical assessment. Key findings: Meena's menstrual history confirms oligomenorrhoea (6–7 periods/year). She has a modified Ferriman-Gallwey score of 10 (borderline hirsutism, predominantly chin and lower abdomen). There is no galactorrhoea, no striae, no centripetal obesity, and no scalp hair thinning. Blood pressure is 118/76 mmHg. Thyroid gland is impalpable. Rajan reports normal libido and erections. He had bilateral cryptorchidism managed by orchidopexy at age 3. On examination, both testes are palpable, volume approximately 12 mL bilaterally.

DISCUSSION POINTS

  • What is the most likely working diagnosis for Meena's oligomenorrhoea and what is your differential diagnosis? Rank your differentials by probability given the history so far.
  • What does Rajan's history of bilateral cryptorchidism repaired at age 3 tell you about his risk of subfertility? Which specific parameter on semen analysis would you be most concerned about, and why?
  • Outline the three-pronged infertility workup you would initiate at this point, specifying what you would test for in each partner and in what sequence. Justify your sequence.
Click to reveal Trigger 2: Investigation Results — First Round (discuss previous trigger first!)

Trigger 2: Investigation Results — First Round

Results return one week later. Meena: serum TSH 2.1 mIU/L (normal), prolactin 18 ng/mL (normal), day-3 FSH 6.2 IU/L, day-3 LH 11.8 IU/L (LH:FSH ratio 1.9:1), fasting glucose 5.4 mmol/L. Transvaginal ultrasound: uterus normal. Right ovary: 16 follicles measuring 2–9 mm with peripheral distribution, increased stromal echogenicity, ovarian volume 12 mL. Left ovary: 14 follicles, similar morphology, ovarian volume 11 mL. Serum 17-hydroxyprogesterone (17-OHP): 0.9 ng/mL (normal <2.0 ng/mL). Rajan: semen analysis — volume 2.8 mL, pH 7.4, count 9 million/mL (low), motility 38% (low), normal morphology 4%, round cells 2/HPF. WHO reference ranges (2021): count ≥16 million/mL, motility ≥42%, morphology ≥4%.

DISCUSSION POINTS

  • Apply the Rotterdam 2003 criteria explicitly to Meena's results. Does she satisfy 2 of 3? State which criteria she meets, with the specific findings that confirm each criterion. The 17-OHP result is normal — what diagnosis does this help you exclude and why is this exclusion mandatory?
  • Rajan's semen analysis shows oligo-asthenozoospermia (OAT). Given his history of bilateral orchidopexy, what is the most likely aetiology of his OAT? Does this change the treatment strategy?
  • The couple now has a dual cause of infertility — female (PCOS-related anovulation) and male (OAT). How does the presence of a male factor influence the management of the female factor? Does it change your recommendation for ovulation induction modality?
Click to reveal Trigger 3: The Unexpected Finding — Tubal Assessment (discuss previous trigger first!)

Trigger 3: The Unexpected Finding — Tubal Assessment

Because Rajan's OAT is mild-to-moderate and the couple is keen to try natural conception with ovulation induction first, Dr Preethi proceeds with tubal patency assessment before initiating ovulation induction. HSG is performed. The report reads: 'Right tube fills to the ampulla; there is a soft-tissue filling defect at the right cornual region. No spill from the right tube. Left tube fills and spills freely into the peritoneal cavity. Uterine cavity: normal outline, no filling defects.' Meena is distressed. She asks: 'Does this mean I can never have children naturally?'

DISCUSSION POINTS

  • The right proximal block on HSG could represent either tubal spasm or true cornual obstruction. How would you counsel Meena? What is the next investigation to distinguish between these two possibilities, and what would each finding imply for management?
  • If this finding is confirmed as a true right proximal tubal block (e.g., by selective salpingography), and the left tube is patent, does this change the recommended treatment strategy for this couple? Construct a revised management algorithm.
  • Meena is upset and asks whether she should proceed directly to IVF. What are the arguments for and against IVF as the immediate next step, given that she has: PCOS (anovulation), a right tubal block, and her husband has mild OAT? How do you weigh these factors?
Click to reveal Trigger 4: Ovulation Induction — Decision and Complication (discuss previous trigger first!)

Trigger 4: Ovulation Induction — Decision and Complication

Sonosalpingography confirms the right tube is blocked at the cornual region (likely a proximal polyp or debris — not hydrosalpinx). The left tube is patent. Dr Preethi decides to proceed with ovulation induction using letrozole with Rajan's OAT as mild-moderate and the left tube patent. Meena is started on letrozole 2.5 mg day 2–6 with scheduled intercourse and ultrasound monitoring. On day 12 of her cycle, ultrasound shows: three follicles — right ovary 18 mm, right 20 mm, left 22 mm — and serum oestradiol is 1,840 pmol/L. Meena has mild bloating. Dr Preethi considers the next step.

DISCUSSION POINTS

  • Three follicles have developed in a woman with PCOS on letrozole. What is the specific risk associated with multiple follicle development in ovulation induction (not IVF)? State the two-part management decision Dr Preethi must make: should she administer the hCG trigger or withhold it, and should she proceed with timed intercourse or convert to IUI?
  • PCOS patients are at higher risk of OHSS during ovulation induction than the general population. Explain the pathophysiological reason for this (link to the preantral follicle pool size and AMH). What specific features of PCOS make gonadotrophin-based ovulation induction riskier than letrozole, and what monitoring safeguards are required?
  • Meena asks: 'If this cycle does not result in pregnancy, what are our options going forward?' Outline the escalation pathway — in sequence — for a PCOS couple with mild male factor and one confirmed blocked tube, from least to most invasive treatment.
Click to reveal Trigger 5: Long-Term Perspective — Metabolic Risk Counselling (discuss previous trigger first!)

Trigger 5: Long-Term Perspective — Metabolic Risk Counselling

Two cycles of ovulation induction with letrozole result in ovulation confirmed on progesterone but no pregnancy. The couple decides to pause treatment for 3 months due to work commitments. At their follow-up appointment, Dr Preethi takes the opportunity to counsel Meena about PCOS as a lifelong condition beyond fertility. Meena's fasting glucose is now 5.8 mmol/L (borderline). Her blood pressure is 122/78 mmHg. She has not yet made lifestyle changes. She asks: 'My periods are still irregular. Is that a problem if we are not trying to get pregnant right now? Can I just leave it?'

DISCUSSION POINTS

  • Meena's question — 'Can I just leave it?' — deserves a specific clinical answer. Explain the endometrial cancer risk associated with untreated chronic anovulation in PCOS, including the mechanism (unopposed oestrogen) and the minimum recommended frequency of progestogen-induced withdrawal bleed that is considered protective. What would you prescribe for her during this pause?
  • Her fasting glucose has risen from 5.4 to 5.8 mmol/L over one year. What does this trajectory suggest? What is the appropriate investigation to formally screen for impaired glucose tolerance in PCOS, and at what interval should it be repeated? When would you add metformin to her management?
  • Summarise the three cardinal long-term risks of unmanaged PCOS beyond reproductive years (endometrial, metabolic/diabetic, cardiovascular) and construct a 5-year surveillance plan for Meena, specifying each monitoring parameter and its frequency.

Group Task Assignments

  • Before trigger 1 is opened: write a problem list from the presenting scenario alone, identifying the key clinical problems that need to be addressed for Meena and Rajan separately.
  • After trigger 2: draw a cause-and-effect diagram mapping the insulin resistance — hyperinsulinaemia — androgen excess — anovulation cycle in PCOS. Annotate each step with the clinical finding from Meena's investigation results that supports it.
  • After trigger 3: create a decision tree for the couple's management options at this point, incorporating the dual infertility factors (PCOS anovulation + male OAT + right tubal block). Map each branch to a clinical decision criterion.
  • After trigger 4: role-play the conversation between Dr Preethi and Meena when counselling her about the three-follicle response — specifically how to communicate the multiple pregnancy and OHSS risks without causing unnecessary anxiety or discouraging her from treatment.
  • After trigger 5: write a patient information sheet for Meena about PCOS as a lifelong condition — covering menstrual regulation, metabolic surveillance, and fertility options — in language appropriate for a patient (avoid jargon, use simple analogies).

Learning Issues

Research these questions and bring your findings to the discussion.

  1. [OG30.1] What are the Rotterdam 2003 diagnostic criteria for PCOS and what investigations are required to confirm each criterion and exclude mimics?
  2. [OG30.1] What is the pathophysiological mechanism linking insulin resistance to anovulation and hyperandrogenism in PCOS, and why does obesity worsen this cycle?
  3. [OG28.1] How does the simultaneous presence of male factor and female factor infertility modify the investigation and treatment strategy for a couple?
  4. [OG28.2] How do you distinguish tubal spasm from true proximal tubal occlusion on HSG, and what are the implications of each for management?
  5. [OG28.3] What is the first-line ovulation induction agent in PCOS, what is the evidence base, and what monitoring is required during induction?
  6. [OG28.3] What are the risk factors for OHSS in PCOS and what strategies reduce this risk during ovulation induction?
  7. [OG30.1] What are the endometrial, metabolic, and cardiovascular long-term risks of untreated PCOS, and what is the minimum surveillance schedule?
  8. [OG28.4] When does the clinical situation justify escalation from ovulation induction to IUI to IVF/ICSI, and what factors drive each transition?