Ovarian hyperstimulation syndrome (OHSS) is a complication of ovarian stimulation during IVF infertility treatment. It is associated with the use of human chorionic gonadotropin (hCG) to mature the follicles during the final steps of ovarian stimulation.
The primary mechanism for OHSS is an increase in vascular endothelial growth factor (VEGF) released by the granulosa cells of the follicles. VEGF increases vascular permeability, causing fluid to leak from capillaries. Fluid moves from the intravascular space to the extravascular space. This results in oedema, ascites and hypovolaemia.
The use of gonadotrophins (LH and FSH) during ovarian stimulation results in the development of multiple follicles. OHSS is provoked by the “trigger injection” of hCG 36 hours before oocyte collection. HCG stimulates the release of VEGF from the follicles. The features of the condition begin to develop after the hCG injection.
There is also activation of the renin-angiotensin system. A notable finding in patients with OOH is a raised renin level. The renin level correlates with the severity of the condition.
- Younger age
- Lower BMI
- Raised anti-Müllerian hormone
- Higher antral follicle count
- Polycystic ovarian syndrome
- Raised oestrogen levels during ovarian stimulation
Women are individually assessed for their risk of developing OHSS.
During stimulation with gonadotrophins, they are monitored with:
- Serum oestrogen levels (higher levels indicate a higher risk)
- Ultrasound monitor of the follicles (higher number and larger size indicate a higher risk)
In women at higher risk several strategies may be used to reduce the risk:
- Use of the GnRH antagonist protocol (rather than the GnRH agonist protocol)
- Lower doses of gonadotrophins
- Lower dose of the hCG injection
- Alternatives to the hCG injection (i.e. a GnRH agonist or LH)
Early OHSS presents within 7 days of the hCG injection. Late OHSS presents from 10 days onwards.
Features of the condition include:
- Abdominal pain and bloating
- Nausea and vomiting
- Pleural effusions
- Renal failure
- Peritonitis from rupturing follicles releasing blood
- Prothrombotic state (risk of DVT and PE)
The severity is determined based on the clinical features:
- Mild: Abdominal pain and bloating
- Moderate: Nausea and vomiting with ascites seen on ultrasound
- Severe: Ascites, low urine output (oliguria), low serum albumin, high potassium and raised haematocrit (>45%)
- Critical: Tense ascites, no urine output (anuria), thromboembolism and acute respiratory distress syndrome (ARDS)
Management is supportive with treatment of any complications. This involves:
- Oral fluids
- Monitoring of urine output
- Low molecular weight heparin (to prevent thromboembolism)
- Ascitic fluid removal (paracentesis) if required
- IV colloids (e.g. human albumin solution)
Patients with mild to moderate OHSS are often managed as an outpatient. Severe cases require admission, and critical cases may require admission to the intensive care unit (ICU).
TOM TIP: Haematocrit may be monitored to assess the volume of fluid in the intravascular space. Haematocrit is the concentration of red blood cells in the blood. When the haematocrit goes up, this indicates less fluid in the intravascular space, as the blood is becoming more concentrated. Raised haematocrit can indicate dehydration.
Last updated August 2020