IVF and ART techniques — structured SAQ (15 marks)

(a) Trigger decision (4 marks)

One mark per correct element — agent, dose, route, rationale. [1]

• GnRH agonist trigger — leuprolide or triptorelin 0.2 mg subcutaneously (single bolus) approximately 36 hours before oocyte retrieval.[1][8]
• Not hCG — hCG trigger in this high responder (over 20 follicles, oestradiol over 3000 pg/mL, PCOS) carries a severe OHSS risk of 6 to 12%.[9]
• Rationale (2 of the 3 expected): the GnRH agonist displaces endogenous GnRH from the pituitary and triggers a short, self-limited LH surge lasting 24 to 36 hours, in contrast to hCG which has a 24 to 36-hour half-life and continues to stimulate the granulosa cells for several days. In high responders the agonist trigger virtually eliminates severe OHSS, but it causes a luteal phase defect.[1]

(b) Luteal phase support — why progesterone alone fails (3 marks)

• Regimen: vaginal micronised progesterone 200 mg three times daily (or 400 mg twice daily) starting the day of oocyte retrieval, continued through 10 to 12 weeks of gestation if pregnancy is confirmed.[12]
• Plus intensive LH activity support: a small rescue dose of hCG 1500 IU subcutaneously at oocyte retrieval, or aggressive oestradiol and progesterone supplementation — the precise regimen varies by unit but the principle is to mimic the LH activity that the agonist trigger stripped away.[8]
• Why progesterone alone is insufficient: the agonist trigger produces only a short LH surge (24 to 36 hours), leaving the corpora lutea partially luteolysed. Without LH activity support, progesterone alone gives a pregnancy rate roughly half that of hCG trigger with standard support, because the corpus luteum produces insufficient progesterone and vasoactive mediators to maintain early pregnancy.[1][8]

(c) Fresh or frozen transfer? (3 marks)

• Freeze-all (elective cryopreservation of all suitable embryos) and defer transfer to a subsequent cycle. No fresh transfer in this cycle.[10][2]
• Rationale: even with an agonist trigger, fresh transfer in a high responder compounds OHSS risk because the implantation-initiated hCG from the early pregnancy re-stimulates the granulosa cells. Freeze-all decouples the OHSS exposure from the luteal phase and, in hyper-responders, is associated with higher live birth than fresh transfer.[2][10]
• Plus: deferred transfer allows the endometrium to recover from the high-oestradiol environment; FET preparation typically uses programmed cycles with oestradiol and progesterone, giving endometrial and clinical outcomes comparable to fresh in non-OHSS cycles.[2]

(d) Severe OHSS — immediate management (3 marks)

• Admit to a high-dependency or gynaecology ward with daily weights, abdominal girth, fluid balance, oxygen saturation.[9]
• IV crystalloid (sodium chloride 0.9% or balanced crystalloid) at a maintenance rate, with caution not to overload — pulmonary oedema is a recognised iatrogenic complication; aim for urine output over 30 mL/hour.[9]
• Thromboprophylaxis with LMWH (e.g. enoxaparin 40 mg subcutaneously daily) for the duration of admission — severe OHSS carries a thromboembolic risk of 1 to 2% from haemoconcentration and ascites.[9]
• Paracentesis for tense ascites causing respiratory compromise or worsening oliguria; dopamine infusion (2 to 4 micrograms/kg/min) if persistent oligo-anuria despite fluids.[9]
• Monitor: serum electrolytes, haematocrit, creatinine, LFTs, coagulation; transvaginal ultrasound for ovarian size; chest X-ray and pulse oximetry if respiratory symptoms.[9]

(e) The one modifiable risk factor for next time (2 marks)

• Weight loss — a 5 to 10% loss of body weight in overweight or obese women with PCOS reduces the ovarian response to gonadotropin, improves oocyte and embryo quality, and lowers the OHSS risk for the next cycle. Metformin 1500 to 2000 mg daily can be considered as an adjunct in PCOS with insulin resistance, but lifestyle modification is the cornerstone.[9]