Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Ovarian hyperstimulation syndrome
Obstetrics and gynaecology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
!
Severe OHSS is a capillary-leak emergency
Rapid fluid shift can cause ascites, pleural effusion, haemoconcentration, renal impairment, respiratory compromise and venous or arterial thrombosis, sometimes at unusual sites.
Action: Assess airway, breathing, circulation, urine output and thrombosis symptoms; involve the fertility and gynaecology teams urgently, obtain severity investigations, admit when criteria are met and escalate organ dysfunction to critical care.
Overview
Prevent, recognise, grade and manage ovarian hyperstimulation syndrome using the 2026 RCOG classification, with early escalation for capillary leak, organ dysfunction and thrombosis.
OHSS occurs when a stimulated ovary releases vasoactive mediators that increase capillary permeability. Protein-rich fluid leaves the intravascular space for the peritoneal and sometimes pleural cavities. The person can therefore be visibly fluid overloaded while intravascularly depleted. Haemoconcentration, reduced renal perfusion, electrolyte disturbance and a strongly prothrombotic state explain the dangerous complications and why indiscriminate diuresis can worsen disease.
Risk assessment begins before stimulation. PCOS, high AMH or AFC, younger age, previous OHSS and a large follicular response increase risk, but any stimulated patient may be affected. Use individualised gonadotrophin dosing and the current ESHRE prevention framework. Antagonist protocols, an appropriate trigger strategy, cancellation and freezing all embryos when response is excessive reduce risk; a freeze-all strategy prevents pregnancy-driven late worsening but does not instantly reverse early disease.
Aetiology
01
Ovarian stimulation
Exogenous gonadotrophins recruit a follicular cohort, with risk rising as ovarian response and follicle number increase.
02
hCG exposure
An exogenous hCG trigger drives early OHSS, while endogenous pregnancy hCG drives late and often more prolonged disease.
03
High-response phenotype
PCOS, high AMH or AFC, younger age and previous OHSS identify increased susceptibility but do not account for every case.
04
Fresh pregnancy cycle
Embryo transfer followed by implantation can sustain mediator production, which is why early symptoms before transfer prompt freeze-all.
Pathophysiology
1
VEGF-mediated permeability
Stimulated ovaries release vasoactive mediators that loosen endothelial barriers and allow protein-rich plasma to leave vessels.
2
Third spacing
Ascites and pleural fluid accumulate while circulating volume contracts, impairing renal perfusion and concentrating blood cells.
3
Hypercoagulability
Haemoconcentration, inflammation, reduced mobility, high oestrogen and pregnancy combine to raise arterial and venous thrombosis risk.
4
Pressure effects
Tense ascites restricts diaphragmatic movement and elevates renal venous and intra-abdominal pressure, worsening respiration and oliguria.
Clinical features and red flags
Mild OHSS
Mild abdominal pain or bloating with ovaries usually under 8 cm and haematocrit under 0.40, without ultrasound ascites or organ dysfunction.
Moderate OHSS
Moderate pain, nausea or vomiting and ultrasound ascites, with ovaries usually 8 to 12 cm and haematocrit below 0.45.
Severe OHSS
Any clinical ascites, significant haemoconcentration, hypoalbuminaemia, hyponatraemia, hyperkalaemia, low osmolality or specified oliguria places the patient in the severe category.
Critical OHSS
Tense ascites or pleural effusion, haematocrit over 0.55, white cells over 25 × 10^9/L, anuria, thromboembolism or ARDS requires high-dependency or critical-care assessment.
Late pregnancy-associated OHSS
Symptoms beginning about 10 days or more after trigger, particularly with a positive pregnancy, are driven by endogenous hCG and may persist longer.
Red flags requiring action
Dyspnoea, hypoxia, chest pain, haemoptysis or a large pleural effusion may indicate respiratory compromise or pulmonary embolism.
Unilateral leg swelling, focal neurological deficit, severe headache, visual symptoms or neck swelling may represent venous or arterial thrombosis at a typical or unusual site.
Oliguria below 300 mL in 24 hours or below 30 mL/hour, anuria, rising creatinine or a positive fluid balance over 1 litre requires urgent review.
Investigations
01Serial observations and fluid balanceFirst step
Why
Detect respiratory, circulatory and renal deterioration.
Interpretation and limitations
Falling oxygen saturation, tachycardia, hypotension, urine below 30 mL/hour or a positive balance over 1 litre warrants prompt reassessment and escalation.
02Full blood count and haematocrit
Why
Measure haemoconcentration and support severity classification while following trend.
Interpretation and limitations
Haematocrit over 0.45 is severe and over 0.55 critical; white cells over 25 × 10^9/L is critical, but infection remains a differential when clinically supported.
03Urea, creatinine, electrolytes, osmolality and albumin
Why
Identify intravascular depletion, renal impairment and capillary-leak biochemistry.
Interpretation and limitations
Sodium below 135, potassium over 5, osmolality below 282 or albumin below 35 meets severe criteria; trends and urine output guide fluid and critical-care decisions.
04Pelvic ultrasound
Why
Assess ascites, ovarian enlargement and early pregnancy location and exclude selected pelvic alternatives.
Interpretation and limitations
Ascites supports at least moderate disease; ovarian size does not override a severe biochemical or organ feature and can correlate poorly after follicle aspiration.
Differential diagnosis
01
Adnexal torsion
Enlarged stimulated ovaries increase torsion risk; sudden localised pain and nausea should not be explained away by OHSS.
02
Ovarian bleeding or cyst rupture
Acute focal pain, falling haemoglobin, peritoneal signs, shoulder-tip pain or haemodynamic instability after oocyte retrieval may indicate significant intra-abdominal haemorrhage.
03
Ectopic or heterotopic pregnancy
A positive test with pain or bleeding requires pregnancy-location assessment even when an intrauterine gestation is seen after assisted conception.
04
Pelvic infection
Fever, focal tenderness and inflammatory features after retrieval can indicate infection rather than sterile capillary leak.
05
Other acute abdomen or medical disease
Appendicitis, gastroenteritis, urinary disease, liver disease and primary thromboembolism can resemble or coexist with OHSS and require diagnosis-specific treatment.
Management
01Immediate assessmentGrade severity and exclude mimicsFirst stepSymptoms occur after ovulation induction or IVF stimulation.+
1Record stimulation, trigger, retrieval, transfer and pregnancy timing; assess ABC, oxygen saturation, pain, vomiting, thrombosis symptoms, weight, girth and urine output.
2Obtain severity bloods and pelvic ultrasound, adding respiratory, thrombotic or acute-abdominal investigations from the presentation.
3Classify by the most severe feature, not by ovarian size alone, and contact the treating fertility unit early.
02Outpatient careUse only when stability and access are reliableDisease is mild or moderate, or selected severe disease is stable without an admission criterion.+
1Confirm pain control, adequate oral intake and urine output, reliable transport and follow-up, and understanding of the 24-hour contact and deterioration symptoms.
Complications
01
Venous or arterial thrombosis
Clots can cause pulmonary embolism, stroke or thrombosis at upper-limb, jugular and cerebral sites as well as conventional leg DVT.
02
Renal and electrolyte injury
Intravascular depletion and raised intra-abdominal pressure reduce renal perfusion, causing oliguria, acute kidney injury, hyponatraemia, hyperkalaemia and worsening fluid imbalance.
03
Respiratory failure
Massive ascites, large pleural effusion, pulmonary embolism or acute respiratory distress syndrome can impair diaphragmatic movement, oxygenation and effective ventilation.
04
Pregnancy and treatment disruption
Severe disease can require cancellation or freeze-all, prolonged admission and complex medication decisions during early pregnancy.
Monitoring and follow-up
Record pulse, blood pressure, respiratory rate, oxygen saturation, temperature, weight, abdominal girth, input and urine output at a frequency matched to severity.
Trend haematocrit, white count, creatinine, sodium, potassium, osmolality and albumin; a single reassuring result does not replace clinical follow-up.
Reassess pain location and intensity because torsion, bleeding, infection, ectopic or heterotopic pregnancy can coexist with enlarged ovaries.
Review VTE risk and prophylaxis at every change in admission status, mobility, pregnancy, procedure or bleeding risk.
Continue follow-up until clinical and biochemical resolution and document the prevention plan for any later stimulation.
Special situations
Third-spaced is not intravascularly replete
A patient with ascites and oedema can still be profoundly intravascularly depleted, so perfusion and urine output guide fluids better than appearance alone.
The worst feature sets the grade
One severe biochemical or organ criterion makes the condition severe even when pain is modest or ovarian size is below the usual range.
Pregnancy can prolong the course
Endogenous hCG drives late OHSS, explaining delayed onset, persistence and first-trimester thromboprophylaxis decisions.
Paracentesis treats physiology
Reducing intra-abdominal pressure can improve diaphragmatic movement, renal perfusion and urine output; it is not merely symptom drainage.
Thrombosis may be unusual
OHSS-associated thrombosis can be arterial or venous and occur in upper-limb, neck or cerebral vessels, so neurological or atypical symptoms need urgent attention.
Common pitfalls
01
Reassuring on ovarian size alone after oocyte retrieval despite severe haemoconcentration, oliguria or electrolyte disturbance.
02
Giving NSAIDs for pelvic pain when intravascular depletion and renal impairment are central risks.
03
Using diuretics routinely for oedema or ascites without correcting intravascular volume or seeking specialist advice.
04
Discharging a patient who cannot maintain oral fluids, has uncontrolled pain or lacks reliable urgent follow-up.
05
Missing thrombosis because symptoms occur in the neck, upper limb or nervous system rather than the calf or chest.
06
Proceeding with a fresh embryo transfer despite early OHSS symptoms instead of freezing embryos for interval transfer.
Practice
Two practice questions
Your practice draft is saved in this browser.
Question 1 of 2
0 correct
Obstetrics and gynaecologyOriginal SBA
A severe OHSS threshold
A patient five days after oocyte retrieval has ascites and reduced urine output. Which finding independently meets the 2026 RCOG severe OHSS category?
Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Every person receiving stimulation should receive verbal and written warning information and a 24-hour contact number. Symptoms include abdominal bloating, increasing girth, pain, nausea, vomiting, rapid weight gain, thirst, breathlessness and reduced urine output. Ask the timing of trigger, oocyte retrieval and embryo transfer and whether pregnancy testing is positive. Early symptoms before a planned fresh transfer should lead to avoidance of fresh transfer and cryopreservation of embryos for later use.
RCOG's 2026 severity classification combines symptoms, ovarian size and capillary-leak markers. Mild disease involves bloating or mild pain, ovaries usually under 8 cm and haematocrit under 0.40. Moderate disease involves moderate pain, nausea or vomiting, ultrasound ascites, ovaries usually 8 to 12 cm and haematocrit under 0.45. Ovarian size is supportive, not decisive, particularly after oocyte retrieval when aspiration alters appearance.
Severe OHSS is present if any severe feature exists: clinical ascites, ovaries usually over 12 cm, haematocrit over 0.45, sodium below 135 mmol/L, potassium over 5 mmol/L, albumin below 35 g/L, serum osmolality below 282 mOsm/kg, or urine output below 300 mL per day or 30 mL per hour. Critical features are tense ascites or pleural effusion, haematocrit over 0.55, white cells over 25 × 10^9/L, anuria, thromboembolism or ARDS.
Assessment is clinical and serial. Record observations, oxygen saturation, weight, abdominal girth, hydration, chest findings, fluid input and urine output. Obtain full blood count and haematocrit, urea, creatinine and electrolytes, liver tests, albumin and other tests guided by severity. Ultrasound assesses ascites, ovaries and pregnancy; chest imaging, ECG, blood gas or thromboembolism imaging is symptom led. Consider ovarian torsion, cyst rupture, bleeding, ectopic or heterotopic pregnancy, pelvic infection, appendicitis and other medical causes rather than attributing every symptom to OHSS.
Mild and moderate disease, and selected stable severe cases, can be managed as outpatients if pain is controlled, oral intake and urine output are adequate, follow-up is reliable and deterioration advice is understood. Review stable outpatients every 2 to 3 days with symptoms, observations, weight, girth, fluid balance and repeat bloods as indicated. Admit if follow-up is impossible, pain is uncontrolled, oral fluids cannot be maintained because of nausea or vomiting, or the condition worsens despite outpatient care.
In hospital, use multidisciplinary care with gynaecology and the treating fertility unit; involve physicians, anaesthesia, haematology, respiratory, renal and critical care according to organ effects. Replace intravascular volume judiciously with crystalloids, guided by perfusion and urine output rather than visible oedema alone. Avoid routine diuretics in an intravascularly depleted person. Paracentesis can markedly improve renal and respiratory function when ascites is driving pressure and should be ultrasound guided through an abdominal or transvaginal route.
Thrombosis prevention is central. Perform an individual VTE assessment. All inpatients should receive anti-embolism stockings and LMWH unless contraindicated, and severe outpatients should receive both. A pregnant person with OHSS should receive LMWH throughout the first trimester unless contraindicated; any longer duration is individualised to severity and other risk factors. Suspected thrombosis requires urgent imaging and therapeutic anticoagulation decisions, not merely a prophylactic dose.
Follow until clinical and biochemical resolution. Early disease often improves as exogenous hCG effect wanes, whereas a pregnancy can sustain late disease for weeks. Escalate increasing pain, weight or girth, falling urine output, worsening haemoconcentration, electrolytes, oxygenation or mobility. Communicate pregnancy-safe medication choices and early-pregnancy follow-up, and offer debriefing about how a future stimulation protocol will reduce recurrence risk.
Key points
OHSS is an iatrogenic increase in vascular permeability after ovarian stimulation, driven chiefly by hCG-related ovarian vasoactive mediators including VEGF.
Early OHSS follows the treatment trigger; late OHSS usually begins 10 days or more later and is sustained by endogenous hCG from pregnancy, often making it longer and more severe.
Mild disease has bloating or mild pain, ovaries usually below 8 cm and haematocrit below 0.40; moderate disease adds nausea or vomiting and ultrasound ascites, with ovaries usually 8 to 12 cm and haematocrit below 0.45.
Any severe feature defines severe disease: clinical ascites, haematocrit above 0.45, sodium below 135 mmol/L, potassium above 5 mmol/L, albumin below 35 g/L, serum osmolality below 282 mOsm/kg or oliguria below 300 mL/day or 30 mL/hour.
Critical OHSS includes tense ascites or pleural effusion, haematocrit above 0.55, white cells above 25 × 10^9/L, anuria, thromboembolism or ARDS.
Manage mild or moderate disease and selected stable severe disease as an outpatient only when pain and intake are controlled, follow-up is reliable and urgent advice is available; review stable outpatients every 2 to 3 days.
Avoid NSAIDs because renal perfusion is vulnerable. Use paracetamol and, when necessary, pregnancy-compatible opioids; prescribe LMWH thromboprophylaxis according to severity, pregnancy and individual risk.
Tense or rapidly increasing ascites, severe pain, persistent vomiting, syncope, haemodynamic change or inability to maintain oral fluid intake supports admission.
Investigate dyspnoea, hypoxia, chest pain, limb swelling or neurological symptoms.
Interpretation and limitations
Pleural effusion may reflect capillary leak, but pulmonary embolism or thrombosis at an unusual site must be actively excluded when symptoms indicate.
06Pregnancy testing and early-pregnancy assessment
Why
Recognise endogenous hCG as a driver and evaluate ectopic or heterotopic pregnancy.
Interpretation and limitations
Pregnancy predicts a potentially prolonged late course; pain or bleeding still needs location assessment rather than attribution to enlarged ovaries alone.
2
Use paracetamol or pregnancy-compatible opioid if required, avoid NSAIDs, assess VTE risk and prescribe stockings or LMWH when indicated.
3Review every 2 to 3 days while stable, sooner for any deterioration, repeating weight, girth, fluid balance and bloods according to severity.
03Admission and escalationSupport organs and prevent thrombosisEscalationPain is uncontrolled, fluids cannot be maintained, follow-up is unsafe, disease is worsening, or severe organ or critical features are present.+
1Admit under gynaecology with fertility-unit input, measure strict input and output, use anti-embolism stockings and LMWH unless contraindicated, and involve other specialties early.
2Restore intravascular volume judiciously, avoid NSAIDs and routine diuretics, and manage electrolyte, respiratory or renal complications with critical-care support when needed.
3Arrange ultrasound-guided paracentesis for pressure-related severe pain, respiratory compromise or oliguria despite appropriate volume replacement.
04Prevention and follow-upStop progression and plan safer future treatmentA high response is recognised or OHSS is resolving.+
1If early symptoms occur before fresh embryo transfer, do not proceed with fresh transfer; cryopreserve embryos for an interval frozen transfer.
2Continue review until symptoms, urine output, observations and laboratory abnormalities resolve; if pregnancy occurs, provide LMWH through the first trimester unless contraindicated and individualise any longer duration.
3Debrief the episode and document high-risk response, trigger and preventive modifications for any future stimulation cycle.
Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
Prevents OHSS-associated venous thromboembolism in hospitalised or severe outpatient disease and throughout the first trimester when OHSS accompanies pregnancy.
Low-molecular-weight heparin
Use the prophylactic LMWH dose specified by the local pregnancy and VTE protocol, adjusted for current weight and renal function; suspected or confirmed thrombosis requires a separate therapeutic regimen.
Assess active bleeding, platelet history, renal impairment, planned procedures and neuraxial anaesthesia. Coordinate timing around paracentesis or surgery and distinguish prophylaxis from treatment.
Provides first-line analgesia for OHSS pain when oral treatment is suitable and urgent alternative pathology has been considered.
Paracetamol
Give 500 mg to 1 g orally every 4 to 6 hours as needed, maximum 4 g in 24 hours for a suitable adult; use a lower maximum for low body weight, hepatic risk or local policy.
Check combination products, low body weight and liver disease. Avoid substituting NSAIDs because renal perfusion may be compromised, and reassess escalating or localised pain.
Supports intravascular volume when admitted OHSS causes depletion, haemodynamic compromise or inadequate oral intake.
Intravenous crystalloid
Give cautious, reassessment-led boluses or maintenance according to observations, perfusion, urine output, electrolytes and critical-care advice rather than a fixed large-volume regimen.
Third-spacing can worsen ascites and pleural effusion even while intravascular depletion persists; avoid reflex fluid loading without repeated examination and strict input-output monitoring.
Drain ascites under ultrasound guidance when it causes severe pain or distension, respiratory compromise or oliguria despite appropriate intravascular volume replacement.