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Management of
Ovarian
Hyperstimulation
Syndrome
By
Dr. A. A. Abudu
Outline
• Introduction
• Epidemiology
• Pathophysiology
• Clinical presentation
• Clinical assessment
• Treatment
• OHSS a...
Introduction
• Ovarian hyperstimulation syndrome (OHSS)
was first described in 1943 by Rydberg et al.
as a loss of control...
Introduction
• Ovarian hyperstimulation syndrome (OHSS)
is an important and potentially fatal
complication of ovulation in...
Introduction
• Mainly associated with multifollicular
response seen with gonadotrophin
stimulation but may also occur foll...
Epidemiology
• True incidence is unknown - classification
schemes, underdiagnosis
• Mild OHSS: 20 – 33% of IVF cycles
• Mo...
Pathophysiology
Pathophysiology of symptoms
Clinical presentation
• OHSS is generally a self-limiting disorder and
symptoms typically resolve spontaneously
within 7 t...
Clinical presentation
• Early OHSS occurs within 10 days of hCG
trigger and reflects ovarian response to
exogenous hormone...
Clinical presentation
• Symptoms:
• Abdominal bloating
• Nausea and vomiting
• Abdominal pain
• Abdominal distension
• Wei...
Clinical presentation
• Complications:
• Ascites, pleural/pericardial effusions
• Electrolyte abnormalities (Na , K )
• Hy...
Clinical presentation
Clinical presentation
• Differential diagnoses:
• Ovarian cyst accidents (torsion, haemorrhage,
rupture)
• Pelvic infectio...
Clinical assessment
• History, timing of ovulation induction
• Full systemic examination
• Baseline weight and abdominal g...
Clinical assessment
Treatment
• Management is generally supportive until
spontaneous resolution occurs
• May require hospitalization for sever...
Treatment
• Patient education – vital component
• Discontinue hCG for luteal support,
progesterone may be used
• Avoid str...
Treatment – outpatient care
• Adequate hydration – drink to thirst
• Antiemetics – metoclopramide, cyclizine
• Analgesics ...
Treatment – outpatient care
• Symptom monitoring – appearance of new
symptoms or worsening of existing ones
• Daily weight...
Treatment - hospitalisation
• Usually required for severe cases, poor
symptom control, social considerations
• Multidiscip...
Treatment - hospitalisation
•Fluid management:
• Oral fluid intake preferable to intravenous
• 2-3L/day of fluid with stri...
Treatment - hospitalisation
• Fluid management:
• Crystalloids – use of physiological saline or
dextrose in normal saline ...
Treatment - hospitalisation
•Fluid management:
• Diuretics avoided due to depletion of
intravascular volume. May have a ro...
Treatment - hospitalisation
• Paracentesis (ultrasound-guided):
• ascites causing pain, compromised pulmonary
function or ...
Treatment - hospitalisation
• Thromboprophylaxis with TED stockings,
low-molecular weight heparin (SC
Enoxaparin 40mg dail...
Treatment - hospitalisation
• Chest tube drainage of significant pleural
effusion that persists after paracentesis
• Surgi...
Treatment - hospitalisation
• Monitoring of symptoms
• Daily weighing and abdominal girth
measurement
• Vital signs, oxyge...
Treatment - hospitalisation
• Serial full blood count, electrolytes, urea
and creatinine – daily
• Liver function tests, c...
Treatment - hospitalisation
OHSS and pregnancy
• Severe OHSS commonly associated with
pregnancy
• Pregnancy may continue normally despite
OHSS
• No ev...
Prevention
• Begins with identification of patients at-
risk
• Prior history of OHSS
• Young age
• Low BMI
• Polycystic ov...
Prevention
• Increased antral follicle count; ≥ 24
• High anti-Mullerian hormone; ≥ 3.36ng/ml
• Multiple follicles (>14 fo...
Prevention – primary
• Reduced dose of gonadotrophins - chronic
low-dose step-up protocol, limited ovarian
stimulation, av...
Prevention – primary
• Reduced duration of exposure to
gonadotrophins – mild stimulation
protocol (clomiphene, GnRH-antago...
Prevention – primary
• No use of hCG for luteal support
• In-vitro maturation of oocytes
• Use of insulin-sensitizing agen...
Prevention – secondary
• Coasting – withhold further gonadotropin
stimulation and delay hCG administration
until oestradio...
Prevention – secondary
• Cycle cancellation – waste of resources,
risk of spontaneous ovulation
• Reduced hCG doses as ovu...
Prevention – secondary
•Alternative ovulation triggers –
• GnRH-agonists in antagonist-stimulated
cycles – likelihood of c...
Prevention – secondary
• Cryopreservation of oocytes – prevents
late OHSS and exacerbation of early OHSS
by pregnancy
• Do...
Prevention – secondary
• Intravenous albumin, hydroxyethyl starch
(HES) – bind vasoactive agents, increases
plasma oncotic...
Prevention
Conclusion
• Ovarian hyperstimulation syndrome is a
mostly iatrogenic and self-limiting disorder
• Good clinical acumen re...
References
• Khalid S, Gray T, Hashim SS. Ovarian hyperstimulation
syndrome. InnovAiT: Education and inspiration for gener...
Management of ovarian hyperstimulation syndrome
Management of ovarian hyperstimulation syndrome
Management of ovarian hyperstimulation syndrome
Management of ovarian hyperstimulation syndrome
Management of ovarian hyperstimulation syndrome
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Concise discussion of the management options for ovarian hyperstimulation syndrome, a complication of ovulation induction/assisted reproduction

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Management of ovarian hyperstimulation syndrome

  1. 1. Management of Ovarian Hyperstimulation Syndrome By Dr. A. A. Abudu
  2. 2. Outline • Introduction • Epidemiology • Pathophysiology • Clinical presentation • Clinical assessment • Treatment • OHSS and pregnancy • Prevention
  3. 3. Introduction • Ovarian hyperstimulation syndrome (OHSS) was first described in 1943 by Rydberg et al. as a loss of control over the intended therapeutic stimulation of the ovaries • In 1951, the first fatal case of OHSS was reported
  4. 4. Introduction • Ovarian hyperstimulation syndrome (OHSS) is an important and potentially fatal complication of ovulation induction • Generally self-limiting and varies from mild to severe life-threatening symptoms that may require hospital admission in up to 1.9% of all OHSS cases
  5. 5. Introduction • Mainly associated with multifollicular response seen with gonadotrophin stimulation but may also occur following use of clomiphene citrate, gonadotrophin- releasing hormone and rarely, spontaneous conception cycles
  6. 6. Epidemiology • True incidence is unknown - classification schemes, underdiagnosis • Mild OHSS: 20 – 33% of IVF cycles • Moderate OHSS: 3 – 6% • Severe OHSS: 0.1 – 2%
  7. 7. Pathophysiology
  8. 8. Pathophysiology of symptoms
  9. 9. Clinical presentation • OHSS is generally a self-limiting disorder and symptoms typically resolve spontaneously within 7 to 10 days • Can be described as early or late depending on time of onset of symptoms
  10. 10. Clinical presentation • Early OHSS occurs within 10 days of hCG trigger and reflects ovarian response to exogenous hormone • Late OHSS occurs more than 10 days after hCG trigger (≈7 days after ET), response to endogenous hCG from pregnancy – prolonged course, risk of severity
  11. 11. Clinical presentation • Symptoms: • Abdominal bloating • Nausea and vomiting • Abdominal pain • Abdominal distension • Weight gain • Dyspnoea • Oliguria (or anuria)
  12. 12. Clinical presentation • Complications: • Ascites, pleural/pericardial effusions • Electrolyte abnormalities (Na , K ) • Hypovolemic shock and acute renal failure • Thromboembolic events and disseminated intravascular coagulopathy (DIC) • Ovarian torsion, rupture • Adult respiratory distress syndrome (ARDS)
  13. 13. Clinical presentation
  14. 14. Clinical presentation • Differential diagnoses: • Ovarian cyst accidents (torsion, haemorrhage, rupture) • Pelvic infection • Intra-abdominal haemorrhage • Ectopic pregnancy • Appendicitis
  15. 15. Clinical assessment • History, timing of ovulation induction • Full systemic examination • Baseline weight and abdominal girth • Laboratory investigations – full blood count, electrolytes, urea and creatinine, liver function tests, clotting profile • Imaging – ultrasound scan, chest X-ray
  16. 16. Clinical assessment
  17. 17. Treatment • Management is generally supportive until spontaneous resolution occurs • May require hospitalization for severe to critical OHSS and moderate OHSS with poor symptom control
  18. 18. Treatment • Patient education – vital component • Discontinue hCG for luteal support, progesterone may be used • Avoid strenuous exercise and sexual intercourse – risk of torsion
  19. 19. Treatment – outpatient care • Adequate hydration – drink to thirst • Antiemetics – metoclopramide, cyclizine • Analgesics – paracetamol, codeine. Avoid NSAIDs – risk of renal compromise • Monitoring of care – review every 2-3 days usually adequate
  20. 20. Treatment – outpatient care • Symptom monitoring – appearance of new symptoms or worsening of existing ones • Daily weight measurement – >2pounds/day (≈1kg/day) • Monitoring of urinary output • Urgent clinical review may be required
  21. 21. Treatment - hospitalisation • Usually required for severe cases, poor symptom control, social considerations • Multidisciplinary care, intensive care • Mainly analgesics and antiemetics, fluid management, thromboprophylaxis and treatment of complications
  22. 22. Treatment - hospitalisation •Fluid management: • Oral fluid intake preferable to intravenous • 2-3L/day of fluid with strict fluid balance • Urine output >20-30ml/hr • Avoid worsening third-space fluid shift • Correction of hypovolaemia, hypotension and haemoconcentration
  23. 23. Treatment - hospitalisation • Fluid management: • Crystalloids – use of physiological saline or dextrose in normal saline preferred over ringer’s lactate – hyponatraemia • Colloids like albumin, mannitol, dextran, hydroxyethyl starch (HES) may be required for plasma expansion
  24. 24. Treatment - hospitalisation •Fluid management: • Diuretics avoided due to depletion of intravascular volume. May have a role in cases of persistent oliguria despite adequate intravascular volume expansion and normal intraabdominal pressure (after paracentesis)
  25. 25. Treatment - hospitalisation • Paracentesis (ultrasound-guided): • ascites causing pain, compromised pulmonary function or oliguria/anuria unresponsive to appropriate fluid management • Reduced intraabdominal pressure renal perfusion • Intravenous colloid replacement
  26. 26. Treatment - hospitalisation • Thromboprophylaxis with TED stockings, low-molecular weight heparin (SC Enoxaparin 40mg daily) and heparin (SC 5,000 IU 12hourly) • Treatment of thromboembolism with low- molecular weight heparins
  27. 27. Treatment - hospitalisation • Chest tube drainage of significant pleural effusion that persists after paracentesis • Surgical intervention – ovarian torsion • Monitoring of care
  28. 28. Treatment - hospitalisation • Monitoring of symptoms • Daily weighing and abdominal girth measurement • Vital signs, oxygen saturation – 2-8 hourly • Daily physical examinations • Intake/output monitoring
  29. 29. Treatment - hospitalisation • Serial full blood count, electrolytes, urea and creatinine – daily • Liver function tests, clotting profile – as necessary • Ultrasound scans, echocardiogram, chest X-rays – as required
  30. 30. Treatment - hospitalisation
  31. 31. OHSS and pregnancy • Severe OHSS commonly associated with pregnancy • Pregnancy may continue normally despite OHSS • No evidence of increased risk of congenital abnormalities
  32. 32. Prevention • Begins with identification of patients at- risk • Prior history of OHSS • Young age • Low BMI • Polycystic ovarian syndrome (PCOS) • Use of GnRH-agonists
  33. 33. Prevention • Increased antral follicle count; ≥ 24 • High anti-Mullerian hormone; ≥ 3.36ng/ml • Multiple follicles (>14 follicles with diameter of 11mm) • Rapidly rising serum oestradiol level • Prevention can be primary or secondary
  34. 34. Prevention – primary • Reduced dose of gonadotrophins - chronic low-dose step-up protocol, limited ovarian stimulation, avoiding FSH on day of hCG trigger; response monitored with serial ultrasound scans and serum oestradiol levels (2,500pg/ml threshold for risk)
  35. 35. Prevention – primary • Reduced duration of exposure to gonadotrophins – mild stimulation protocol (clomiphene, GnRH-antagonists) • Use of GnRH-antagonist protocols (cf agonist) for controlled ovarian stimulation
  36. 36. Prevention – primary • No use of hCG for luteal support • In-vitro maturation of oocytes • Use of insulin-sensitizing agents like metformin in patients with PCOS
  37. 37. Prevention – secondary • Coasting – withhold further gonadotropin stimulation and delay hCG administration until oestradiol levels plateau or decrease significantly. No reduction in incidence of moderate and severe OHSS in RCTs. Delay usually less than 3 days.
  38. 38. Prevention – secondary • Cycle cancellation – waste of resources, risk of spontaneous ovulation • Reduced hCG doses as ovulation trigger – 5,000 IU cf 10,000IU used successfully in some centres
  39. 39. Prevention – secondary •Alternative ovulation triggers – • GnRH-agonists in antagonist-stimulated cycles – likelihood of clinical pregnancy lower • recombinant LH – lower pregnancy rate, poor cost/benefit ratio
  40. 40. Prevention – secondary • Cryopreservation of oocytes – prevents late OHSS and exacerbation of early OHSS by pregnancy • Dopamine agonists like cabergoline reverse VEGF-mediated vascular permeability. Started on day of hCG trigger as 0.5mg for 8 days.
  41. 41. Prevention – secondary • Intravenous albumin, hydroxyethyl starch (HES) – bind vasoactive agents, increases plasma oncotic pressure • GnRH-antagonist salvage – reduction or plateau of rising oestradiol levels mid-cycle
  42. 42. Prevention
  43. 43. Conclusion • Ovarian hyperstimulation syndrome is a mostly iatrogenic and self-limiting disorder • Good clinical acumen required to diagnose • Multiple options of prevention available to reduce incidence and limit severity
  44. 44. References • Khalid S, Gray T, Hashim SS. Ovarian hyperstimulation syndrome. InnovAiT: Education and inspiration for general practice. 2015 Sep 1;8(9):531-8. • Mahajan N. Ovarian hyperstimulation syndrome. Int J Infertil Fetal Med. 2013 Sep;4:71-8. • Onofriescu AL, Luca A, Bors A, HOLICOV M, ONOFRIESCU M, VULPOI C. Principles of diagnosis and management in the ovarian hyperstimulation syndrome. Curr Health Sci J. 2013 Jul 1;39:187-92. • Kaur H. Prevention of Ovarian Hyperstimulation Syndrome. Journal of Infertility and Reproductive Biology. 2013;1(4):63-8. • Smith V, Osianlis T, Vollenhoven B. Prevention of Ovarian Hyperstimulation Syndrome: A Review. Obstetrics and gynaecology international. 2015 May 14;2015.
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Concise discussion of the management options for ovarian hyperstimulation syndrome, a complication of ovulation induction/assisted reproduction

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