O&G Vivas · Reproductive endocrinology & infertility — fertility-treatment complications
OHSS after IVF trigger — structured oral station (12 minutes)
FRANZCOG oral-format station on OHSS: severity grading using Golan-REI criteria, the acute resuscitation bundle, the prophylaxis ladder with the agonist trigger as the most effective single intervention, and counselling on long-term ovarian function. Scored against the eight published RANZCOG oral domains.
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Station format
4 minutes reading, 12 minutes examination, 20 marks, global scoring. The eight published RANZCOG oral domains apply: history and examination; investigations and interpreting results; treatment and management; clinical knowledge; complex, urgent or unusual clinical presentations; rapport with patient, support person or colleague; respect; communication skills. OHSS is a clinical-knowledge and treatment-management station with an embedded communication probe on prognosis.[1][2]
Reveal the examiner script and model responsesShowHide
Opening prompt — "Tell me what is wrong with this patient and how you will manage her."
Model response — open with severity grading, then immediate action, then the why: [1][2]
- "This is severe OHSS by the Golan classification with the REI modification. She meets the criteria: clinical ascites, oliguria under 500 mL per 24 hours, haematocrit 0.51 (severe haemoconcentration), weight gain 4 kg, palpable ovaries to the umbilicus. She is on the cusp of critical disease — the hypotension and tachycardia suggest impending circulatory compromise."[1]
- "I will admit her to a monitored bed, secure two large-bore cannulae, send FBC, U&E, LFTs, coagulation and a beta-hCG, catheterise for hourly urine output, and start with crystalloid resuscitation. If she remains hypotensive I switch to colloid — albumin or hydroxyethyl starch. I will start LMWH thromboprophylaxis, which is mandatory in severe disease, and arrange ultrasound-guided paracentesis of the tense ascites — the most effective single intervention for tense ascites with respiratory compromise."[2]
- "The disease must run its course because the hCG trigger has already activated the cascade. My job is supportive: correct intravascular depletion, prevent thrombosis, relieve the ascites, and watch for progression to critical disease."[1]
Examiner is listening for: severity grade with named criteria, named agents and doses, the OHSS paradox (volume expand not diuretics), LMWH mandatory, and paracentesis as the most effective single intervention. [1][2]
Probe 1 — "What would you have done differently in the cycle before trigger?"
- "In hindsight this cycle had multiple red flags: PCOS, AMH 48 pmol/L, 28 follicles on trigger day, oestradiol 4800 pg/mL. The most effective single intervention to prevent severe OHSS in this patient would have been to switch the trigger from hCG 10 000 IU to a GnRH agonist trigger (leuprolide 0.5 to 1 mg subcutaneously or triptorelin 0.2 mg) in this GnRH antagonist cycle, and to freeze all embryos for transfer in a subsequent unstimulated cycle. Humaidan 2013 (Fertil Steril) showed severe OHSS near zero with this combination."[5][6]
- "If the couple cannot accept freeze-all — personal, religious or financial reasons — I would use hCG trigger at a reduced dose (5000 IU) plus prophylactic cabergoline 0.5 mg orally daily for 5 to 8 days from the day of trigger. Cabergoline is a dopamine agonist that reduces VEGFR-2 phosphorylation on endothelial cells and halves moderate-to-severe OHSS in high responders. Carizza 2008 (Fertil Steril) and the Tang 2012 Cochrane review support this."[3][4]
- "Earlier in the cycle, I could also have started at low-dose gonadotropin (under 150 IU per day) with a step-up protocol, recognising that PCOS is the single biggest patient-level risk factor."[6]
Probe 2 — "She suddenly develops acute right iliac fossa pain. What now?"
- "Acute unilateral pain in a patient with enlarged ovaries is ovarian torsion until proven otherwise. I will arrange urgent transvaginal ultrasound with Doppler to look for reduced or absent ovarian blood flow, keep her nil by mouth, give IV fluids and analgesia, and inform the on-call gynaecology consultant. If Doppler is non-diagnostic but the clinical suspicion is high, I will proceed to laparoscopic detorsion with ovarian preservation, NOT oophorectomy. These are reproductive-age women and the ovary can recover after detorsion."[1][2]
Probe 3 — "Why is the haematocrit the most useful dynamic marker?"
- "The haematocrit reflects the degree of intravascular depletion. In OHSS the capillaries leak plasma protein and fluid into the third space, leaving the red cells behind in the intravascular space. The haematocrit rises in proportion to the leak. The Golan criteria use the haematocrit to distinguish mild or moderate (under 0.45), severe (0.45 to 0.55) and critical (over 0.55). The trend over hours is more useful than any single number."[1][2]
Probe 4 — "She is anxious and asks if she will be able to have a baby. What do you say?"
This is a scored communication domain, not a courtesy. [1]
- Move to her eye level, use her name, brief plainly: "You have severe OHSS, a complication of the hormone treatment we used. The complication is treatable and most women recover fully within 1 to 2 weeks. Your long-term fertility is not affected — the ovaries are not damaged, and we will adjust the next cycle to prevent this happening again."
- Acknowledge her fear, commit to a debrief with her partner afterwards, and explain that you will keep her fully informed at every step. Avoid jargon, avoid giving false reassurance about short-term improvement.[1]
Probe 5 — "What is the long-term risk of recurrence?"
- "Recurrence risk is high in subsequent cycles without prophylaxis modification — around 30 per cent if the same protocol is repeated. The risk is dramatically reduced to under 5 per cent with a GnRH antagonist protocol plus agonist trigger plus freeze-all. The single most important change for her next cycle is the trigger choice — hCG is the fuel for the OHSS cascade; replacing it with an agonist trigger stops the cascade at the source."[1][2][5][6]
Probe 6 — "What is the underlying pathophysiology, in one sentence?"
- "hCG binds LH receptors on granulosa cells of multiple corpora lutea, induces VEGF secretion, which activates VEGFR-2 on endothelial cells and disrupts tight junctions, producing capillary leak and third-space fluid shift — the OHSS paradox of total body fluid overload but intravascular depletion."[1]
References6ShowHide
- [1]Kwik M, Karia S, Boothroyd C RANZCOG CREI Consensus Statement on treatment of Ovarian Hyperstimulation Syndrome. Aust N Z J Obstet Gynaecol, 2015.PMID 26279582
- [2]Practice Committee of the American Society for Reproductive Medicine. Prevention of moderate and severe ovarian hyperstimulation syndrome: a guideline. Fertil Steril, 2024.PMID 38099867
- [3]Carizza C, Abdelmassih V, Abdelmassih S, Ravizzini P, et al. Cabergoline reduces the early onset of ovarian hyperstimulation syndrome: a prospective randomized study. Reprod Biomed Online, 2008.PMID 19079957
- [4]Tang H, Mourad SM, Wang A, Zhai SD, et al. Dopamine agonists for preventing ovarian hyperstimulation syndrome. Cochrane Database Syst Rev, 2021.PMID 33851429
- [5]Humaidan P, Polyzos NP, Alsbjerg B, et al. GnRHa trigger and individualized luteal phase hCG support according to ovarian response to stimulation: two prospective randomized controlled multi-centre studies in IVF patients. Hum Reprod, 2013.PMID 23753114
- [6]Leathersich S, Roche C, Hart R Minimising OHSS in women with PCOS. Front Endocrinol (Lausanne), 2025.PMID 40182629