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Mr Parijat Bhattacharjee, Private Consultant Gynaecologist, Harrow, Brentford, Northwood, London, UK / Media / Videos » Ovarian Hyper Stimulation Syndrome: (OHSS)

Ovarian Hyper Stimulation Syndrome: (OHSS)

Ovarian Hyper Stimulation Syndrome: (OHSS)
Posted on: 03-Jul-2026

This video, titled "Ovarian Hyper Stimulation Syndrome: (OHSS)" by Gynae Consultant, outlines the medical definition, pathophysiology, clinical complications, risk factors, and modern management strategies associated with OHSS.

What is OHSS and How Does It Happen?

Ovarian Hyperstimulation Syndrome is one of the most common complications of fertility treatments. It is typically triggered by ovulation induction protocols—ranging from milder oral agents like clomifene citrate and letrozole to superovulation therapies using gonadotropins (such as FSH) during IVF cycles.

  • The Mechanism: OHSS is a "third-space" phenomenon. During a natural LH surge or following an HCG trigger injection, a surge of cytokines—specifically Vascular Endothelial Growth Factor (VEGF)—occurs.
  • Capillary Leakage: This induces rapid neovascularization (new blood vessel growth) and significantly increases capillary permeability. As a result, intravascular fluid and proteins leak out of the bloodstream and accumulate in bodily cavities, primarily the peritoneal cavity (abdomen), pleural space (around the lungs), and rarely, the pericardial space (around the heart).
  • The Timing Peaks: The syndrome typically displays two symptomatic peaks: the first occurs about 7 days after the HCG trigger, and a secondary peak can hit 14 days later if the patient becomes pregnant, as rising natural HCG levels exacerbate the condition.

Clinical Complications

The depletion of intravascular fluid leads to severe physiological imbalances:

  • Thrombosis Risk: As fluid leaves the blood vessels, the blood becomes highly concentrated (hemoconcentration). This spikes the patient's risk for Deep Vein Thrombosis (DVT), Pulmonary Embolism (PE), and in rare instances, arterial thrombosis.
  • Organ Imbalances: Reduced blood volume decreases kidney perfusion, risking pre-renal failure. This triggers anti-diuretic hormone (ADH) release, resulting in hyponatremia (low sodium), which can subsequently activate the renin-angiotensin-aldosterone system, leading to hyperkalemia (high potassium).
  • Physical Distension: Severe fluid shifts cause painful abdominal distension (ascites) and pleural effusions, which manifest as shortness of breath. In extreme cases, it can trigger Adult Respiratory Distress Syndrome (ARDS) or become life-threatening.

Risk Factors and Prevention

Clinicians screen for primary risk factors to identify patients prone to hyper-response:

  • Younger maternal age
  • History of Polycystic Ovary Syndrome (PCOS)
  • High Anti-Müllerian Hormone (AMH) levels or a high Antral Follicle Count (AFC)
  • Retrieval of a high volume of follicles, ovarian edema, or free fluid during egg collection
  • A previous history of OHSS

Preventative Strategies

If a patient is deemed high-risk, clinicians adapt the IVF protocol using an antagonist protocol:

  • Substituting an HCG trigger with a GnRH agonist trigger.
  • Using progesterone instead of HCG for luteal phase support.
  • Utilizing "freeze-all" cycles, where all eggs/embryos are frozen for a delayed embryo transfer to prevent an immediate pregnancy from accelerating symptoms.
  • "Coasting" (withholding or reducing FSH doses) or completely abandoning the cycle.

Clinical Assessment and Management

All patients undergoing ovarian stimulation must be counseled on the warning signs, notably sudden weight gain.

  • Evaluation: Clinical check-ups involve tracking daily weight and abdominal girth, checking for breathlessness, monitoring urinary output, and examining the calves for signs of DVT.
  • Diagnostics: Ultrasound is used to evaluate fluid accumulation (with care taken not to rupture hyperstimulated ovaries), alongside chest X-rays, ECGs, or leg Dopplers if blood clots are suspected. Blood tests monitor rising hematocrit levels, elevated white blood cell counts, renal function (urea/creatinine), and liver enzymes.
  • Treatment: Mild cases are managed in an outpatient setting with close monitoring. Severe cases require inpatient hospitalization.
  • Fluid Management: If urine output drops below 30 mL/hour, a fluid challenge using sodium chloride (without potassium) is administered to protect the kidneys, followed by strict fluid restriction to limit further third-space leaking.
  • Interventions: Diuretics are heavily restricted and only used if acute renal failure develops. In severe scenarios, a paracentesis (abdominal tap) or pleural tap is performed to drain excess fluid, and intravenous albumin is administered to replace leaked proteins.