Give a 10 marker answer for OHSS in gynaecology

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Ovarian Hyperstimulation Syndrome (OHSS) — 10 Mark Answer

Definition

Ovarian Hyperstimulation Syndrome (OHSS) is a completely iatrogenic medical complication unique to stimulatory infertility treatment. It is characterised by ovarian enlargement, extravascular fluid accumulation, and intravascular volume depletion, complicating approximately 0.5–5% of stimulated cycles.

Pathophysiology

OHSS results from the release of proinflammatory mediators in response to human chorionic gonadotrophin (hCG) on a background of supraphysiologic ovarian stimulation. Key mediators include:

Vascular Endothelial Growth Factor (VEGF) — upregulated in granulosa cells by hCG; the primary driver of capillary hyperpermeability
Cytokines, prostaglandins, and histamine — augment the vascular permeability response
Renin-angiotensin system — increased renin/prorenin in follicular fluid and angiotensin-mediated permeability

The result is massive third-space fluid shifts — ascites, pleural and pericardial effusions, and oedema. Women with severe OHSS may lose up to 20% of their circulating volume.

Patterns of Onset

Type	Timing	Cause	Severity
Early OHSS	3–7 days post-hCG trigger	Exogenous hCG	Usually moderate
Late OHSS	12–17 days post-hCG trigger	Endogenous hCG from pregnancy	More severe; worse in multiple gestation

Risk Factors

Patient-related:

Polycystic ovary syndrome (PCOS) or polycystic ovarian morphology
Elevated Anti-Müllerian Hormone (AMH) >3.36–3.4 ng/mL
Previous episode of OHSS
Low body weight, young age

Stimulation-related:

Estradiol (E2) >3,500 pg/mL at time of hCG trigger → 1.5% risk of severe OHSS; E2 >6,000 pg/mL → 38% risk
20 preovulatory follicles → 15% incidence of severe OHSS
≥30 oocytes retrieved → 22.7% incidence of severe OHSS

Classification (Golan/Navot Criteria)

Grade	Features
Mild (Grade 1–2)	Abdominal distension/discomfort; nausea, vomiting, diarrhoea; ovary ≥5 mm
Moderate (Grade 3)	Grade 2 + subclinical ascites on ultrasound (pelvic/perihepatic pocket >9 mm)
Severe (Grade 4–5)	Grade 3 + clinical ascites, hydrothorax, or dyspnoea; Grade 5 additionally includes haemoconcentration, renal insufficiency/oliguria, elevated transaminases, VTE, or ARDS

Clinical Features

Abdominal bloating, pain and distension
Nausea, vomiting
Peripheral oedema, oliguria
Breathlessness, orthopnoea
Investigations show: ↑ haematocrit, ↓ serum osmolality, hyponatraemia, hyperkaliaemia
Venous thromboembolism (VTE) can occur

Management

Outpatient (Mild–Moderate)

Limit activity; daily weight monitoring
Fluid intake ≥1 L/day (electrolyte-balanced)
Daily telephone or clinical follow-up
Admit if weight gain >2 lb/day or symptoms worsen

Indications for Hospitalisation

Inability to tolerate oral hydration, haemodynamic instability, respiratory compromise, tense ascites, haemoconcentration, leukocytosis, hyponatraemia, hyperkaliaemia, abnormal renal/liver function, or decreased O₂ saturation.

Inpatient Management

IV fluids: Crystalloids first-line to correct hypovolaemia, hypotension, electrolyte abnormalities, and oliguria (note: may worsen ascites — careful monitoring essential)
Albumin 25%: 50–100 mg IV every 4–12 hours for intravascular volume expansion if needed
Diuretics: Only after hypovolaemia is corrected
Paracentesis (transvaginal/transabdominal, ultrasound-guided): Relieves pain, hydrothorax, or persistent oliguria; rapid large-volume removal is generally safe in this young population
VTE prophylaxis: Mandatory (LMWH)
ICU consideration: For hyperkaliaemia, renal failure, respiratory failure, or thromboembolism
OHSS is self-limiting: ~7 days in non-pregnant women; 10–20 days in pregnant women

Prevention

Identify High-Risk Patients

PCOS, AMH >3.4 ng/mL, E2 >3,500 pg/mL, ≥25 follicles, or ≥24 oocytes retrieved.

Stimulation Protocol Modifications

Use GnRH antagonist protocols (lower OHSS incidence vs. agonist protocols: ~5% vs. ~9%)
Lower initial gonadotropin doses (150–225 IU) in high-risk patients

Triggering Strategies

GnRH agonist trigger instead of hCG in antagonist cycles → endogenous LH surge with shorter half-life → reduced OHSS risk (preferred for freeze-all cycles)
Dual trigger (GnRH agonist + low-dose hCG) if fresh transfer planned

Coasting

Withhold gonadotropins when E2 >4,500 pg/mL and/or 15–30 mature follicles present
Trigger when E2 falls to <3,500 pg/mL
Cycle cancellation if >30 mature follicles, coasting >4 days, or E2 rises to >6,500 pg/mL during coast

Freeze-All Strategy

Elective frozen embryo transfer (freeze-all) avoids the additional endogenous hCG from a fresh pregnancy, significantly reducing severe OHSS risk

Sources: Berek & Novak's Gynecology; Comprehensive Clinical Nephrology, 7th Edition

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