Management of Ovarian Hyperstimulation Syndrome
Overview
OHSS is a complication of pharmacological ovarian stimulation for assisted reproductive technology (ART), driven by hCG/LH exposure of hyperstimulated ovaries, which triggers VEGF and other proinflammatory mediators. This causes increased vascular permeability, third-space fluid loss (ascites ± pleural/pericardial effusion), hypovolaemia (~20% blood volume loss in severe disease), paradoxical hypo-osmolality/hyponatraemia, and a prothrombotic state. Diagnosis is clinical — there is no diagnostic test. "Early" OHSS presents within 7 days of hCG trigger (excessive ovarian response); "late" OHSS presents ≥10 days after trigger, driven by endogenous hCG from early pregnancy, and tends to be more prolonged/severe.
Risk Factors
Previous OHSS, polycystic ovary syndrome, high antral follicle count, high anti-Müllerian hormone (AMH), and use of a GnRH agonist (rather than antagonist) protocol for controlled ovarian stimulation. Risk is higher when conception occurs, and highest in multiple pregnancy (endogenous hCG effect).
Classification of Severity (RCOG scheme)
- Mild: bloating, mild abdominal pain, ovarian size usually <8cm.
- Moderate: moderate abdominal pain, nausea ± vomiting, ultrasound evidence of ascites, ovarian size usually 8–12cm.
- Severe: clinical ascites (± hydrothorax); oliguria (<300ml/day); haematocrit >0.45; hyponatraemia (Na <135mmol/l); hypo-osmolality (<282mOsm/kg); hyperkalaemia (K >5mmol/l); hypoproteinaemia (albumin <35g/l); ovarian size usually >12cm.
- Critical: tense ascites/large hydrothorax; haematocrit >0.55; white cell count >25,000/ml; oliguria/anuria; thromboembolism; ARDS. Any feature of severe or critical disease classifies the patient in that category, regardless of ovarian size (which is unreliable post-oocyte retrieval).
Management
Mild/moderate and selected severe cases are managed as outpatients: fluid intake to thirst (≥1L/day), input–output charting, paracetamol/opioids for pain (NOT NSAIDs — renal risk), and review every 2–3 days (urgently if worsening). Admission is considered for uncontrolled pain, inability to maintain oral intake, worsening despite outpatient care, social factors, or critical OHSS. Inpatient care involves daily (or more frequent) weight, girth, fluid balance, FBC, U&E, LFTs; oral rehydration is preferred, with IV crystalloid/colloid (e.g. human albumin) for those unable to tolerate oral fluids; diuretics are avoided unless oliguria persists after adequate volume replacement and ascites drainage. Paracentesis (ultrasound-guided, abdominal or transvaginal) is indicated for severe distension/pain, respiratory compromise, or oliguria from raised intra-abdominal pressure. Surgery is reserved for coincident torsion, rupture, or ectopic pregnancy. Severe/critical OHSS and admitted patients require LMWH thromboprophylaxis (individualised duration, continued into pregnancy if conception occurs — often to end of first trimester); moderate OHSS is risk-assessed for stockings/LMWH. Multidisciplinary/critical care input is sought for critical OHSS or persistent haemoconcentration.
OHSS and Pregnancy
Pregnancies complicated by OHSS carry an increased risk of pre-eclampsia and preterm delivery, though not of miscarriage.
High-Yield Exam Points
- Diagnosis of OHSS is clinical — no lab test confirms it; rule out torsion, rupture, ectopic, and infection if severe pain/pyrexia present.
- Early OHSS = within 7 days of trigger (exogenous hCG); late OHSS = ≥10 days (endogenous hCG, pregnancy) — late is usually more severe.
- Classic severe/critical triad to remember: haematocrit >0.45 (severe) / >0.55 (critical), oliguria, hyponatraemia with hypo-osmolality.
- NSAIDs are contraindicated (renal compromise); paracetamol/opioids are first-line analgesia.
- Diuretics are avoided — they worsen intravascular depletion despite ascites.
- GnRH antagonist protocols reduce OHSS incidence versus agonist protocols.
Source: RCOG Green-top Guideline No. 5 (RCOG's current guidance page lists a 4th edition dated 14 April 2026 (previous editions: 1995, 2006, 2016). The 4th edition full text sits behind a BJOG paywall; the clinical content below is drawn from the publicly available 3rd edition (February 2016) full text, whose classification and management framework RCOG's 2026 summary page confirms is unchanged in substance.)
Read the original on rcog.org.uk
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