Ovarian hyperstimulation syndrome — structured SAQ (15 marks)

(a) Severity grading (3 marks)

• Severe OHSS — at minimum one mark for the grade with justification.^[1]
• Justification: she has clinical (large) ascites (shifting dullness, tense abdomen), respiratory compromise (dyspnoea, saturation 95%), haemoconcentration (haematocrit 0.49) and oliguria — these are the severe markers.^[1][2]
• The classification hinge worth stating: the detection of ascites establishes moderate OHSS, and clinical (large) ascites with organ compromise moves her to severe; the critical grade is reserved for grave complications (anuria, thromboembolism, ARDS), which she does not yet have.^[1]
• A further mark for recognising this is likely late OHSS (day 6 after transfer, in a pregnancy cycle): late OHSS depends on pregnancy, is likelier to be severe, and is poorly predicted by the preovulatory response — so check a pregnancy test.^[4]

(b) Pathophysiology (4 marks)

• OHSS is a VEGF-driven hyperpermeability state: the stimulated ovary releases vascular endothelial growth factor, which is the major capillary permeability agent in OHSS ascites (McClure).^[3]
• The capillary leak shifts protein-rich fluid into the third space (ascites, pleural effusion), explaining her tense ascites, weight gain and dyspnoea.^[3][2]
• The same leak depletes the intravascular space, causing haemoconcentration (haematocrit 0.49), hypoalbuminaemia (28 g/L) and reduced organ perfusion (oliguria).^[2]
• hCG is the amplifier — her hCG trigger and now endogenous pregnancy hCG drive VEGF release; this is why late OHSS tracks pregnancy and is more severe. The vicious spiral is hypovolaemia to oliguria/pre-renal AKI and haemoconcentration to thrombosis.^[4][2]

(c) Immediate inpatient management (5 marks)

• Admit and assess volume status rigorously — daily weights, strict fluid balance, abdominal girth; a normal blood pressure hides a depleted intravascular volume, so chase the haematocrit.^[2]
• Fluid strategy: correct intravascular volume with careful crystalloid balanced against colloid/oncotic support (albumin for her low oncotic pressure), titrated to urine output and haematocrit — avoid drowning the third space with saline, which worsens ascites.^[2]
• Thromboprophylaxis: start prophylactic low-molecular-weight heparin and thromboembolic-deterrent stockings — haemoconcentration and hyper-oestrogenism make thromboembolism (including arterial events) the killer complication.^[2]
• Paracentesis (culdocentesis) for her tense ascites: SOGC recommends considering outpatient culdocentesis to prevent disease progression in severe OHSS; Rizk recommends aspiration of ascitic fluid, preferably by the transvaginal route, in severe ascites — it improves renal perfusion, venous return and respiratory function.^[6][2]
• Supportive measures: analgesia, antiemetics, monitor renal function and haematocrit trend, and involve anaesthetics/HDU if oliguria is unresponsive or respiratory compromise worsens.^[2]

(d) Prevention strategy for her next cycle (3 marks)

• Design the cycle for her risk: individualised low-dose gonadotrophin (by age, BMI, antral follicle count, prior response); add metformin in PCOS (may reduce OHSS, SOGC I-A).^[6]
• Use a GnRH antagonist protocol with a GnRH agonist trigger in place of hCG — the single biggest lever against early OHSS; antagonist reduces OHSS without lowering live birth.^[6]
• Secondary prevention and luteal support: cabergoline from the day of trigger reduces OHSS in high-risk women (Cochrane OR 0.32); elective single embryo transfer or freeze-all to remove the pregnancy amplifier of late OHSS; and progesterone, never hCG, for luteal phase support.^[5][6]