Early OHSS
Late OHSS
Related to an exaggerated ovarian
Response to gonadotrophin stimulation
Mainly related to the secretion of placental HCG
<10 days after the ovulation triggering injection of HCG
≥10 days after HCG
Those cases which constitute a combination of the early form and are followed by pregnancy are serious and long-lasting.
Another classification is based on severity of symptoms, clinical presentation and ultrasound findings:
Mild OHSS
Abdominal bloating
Mild abdominal pain
Ovarian size usually <8 cm
Moderate OHSS
Moderate abdominal pain
Nausea ± vomiting
Ultrasound evidence of ascites; ovarian size usually 8–12 cm
Severe OHSS
Clinical ascites (occasionally hydrothorax)
Oliguria Haemoconcentration
Haematocrit >45 %
Hypoproteinaemia; ovarian size usually >12 cm
Critical OHSS
Tense ascites or large hydrothorax
Haematocrit >55 %
White cell count >25,000/ml
Oliguria/anuria
Thromboembolism
Acute respiratory distress syndrome
OHSS is more likely to develop in patients with following risk factors [4]:
1.
Polycystic ovarian syndrome
2.
Elevated baseline AMH
3.
Increased ovarian volume
4.
High antral follicle count (AFC) on baseline scan
5.
Age <30 years
6.
Low body mass index (BMI)
7.
Previous history of OHSS
8.
High doses of FSH used during ovarian stimulation
9.
Large number of oocytes collected (>25)
10.
rapidly rising and/or high oestradiol levels (>17,000 pmol/l)
Diagnosis
1.
History: Nature, duration and severity of symptoms, presence of risk factors if any. Past history of any major medical disorder. Previous history of hyperstimulation
2.
Examinations: body weight and body mass index:
Abdominal circumference
Heart rate
Blood pressure
Cardiovascular system
Respiratory systems
Per abdomen
Pelvic examination should be avoided, as this may induce cyst rupture.
Laboratory Investigations
1.
Full blood count: white cell count and haematocrit
2.
Urea, creatinine and electrolytes (hyponatraemia, hyperkalaemia)
3.
Liver function tests: albumin level
4.
Coagulation profile: elevated fibrinogen and reduced antithrombin III
5.
HCG: if it is 10 days post oocyte retrieval
Radiology
Ultrasound pelvis: For size of ovaries, ascites if any
Ovarian vessel Doppler studies: if suspected ovarian torsion
Others
In particular cases if clinically indicated
Arterial blood gases – to diagnose respiratory failure
D-dimers – elevated
ECG, echocardiogram – pericardial effusion
Chest x-ray
Pleural effusion
Interstitial oedema
CTPA or V/Q scan – definitive diagnosis of pulmonary embolism
OHSS and Complications in Pregnancy
1.
In 1st trimester:
Ovarian torsion (more common between 6 and 10 weeks of pregnancy and with multiple pregnancies)
Abortion
Vanishing twin
Abdominal distention and pain in abdomen
Respiratory distress because of pleural effusion
Dehydration and oliguria
2.
In 2nd trimester:
Development of pregnancy-induced hypertension
Development of glucose intolerance or gestational diabetes mellitus
3.
In 3rd trimester:
Preterm labour
Abruption of placenta
4.
Low birth weight babies with lower Apgar scores
A study by Blandine Courbiere et al. published in 2011 [5] about the outcomes of pregnancy in patients with OHSS showed that the incidence of OHSS requiring hospitalization was 1.14 %.
Early OHSS occurred in 22.5 % of patients and late OHSS in the remaining 77.5 % patients.
In the OHSS group, 10 % had thromboembolic complications.
The miscarriage rate was similar for the OHSS group and the control IVF group.
Incidence of vanishing twin was higher in OHSS group.
There was definitely higher incidence of ovarian torsion and laparoscopy required in OHSS group. Laparoscopy was done in patients with exacerbated abdominal pain and signs of localized peritoneal irritation, and the decision was based on physical examination, clinical judgement and colour Doppler showing decreased or absent venous and/or arterial flow. Incidence was 3.5 times higher in twin pregnancies than singleton pregnancies.
Majority of cases were treated with detorsion of ovary and had an uneventful pregnancy course. Laparoscopic detorsion of ovary is now routinely performed.
Concerning ongoing clinical pregnancies, pregnancy-induced hypertension (PIH) and preterm labour were significantly higher in the OHSS group.
One hypothesis to explain an insufficiency of placentation is a systemic vascular dysfunction with the conjunction between haemoconcentration, hypoxaemia, electrolytic disorder and microthromboembolic events [6].
Kamada et al. observed high concentrations of endothelin-1 (ET-1) in the follicular fluids of women undergoing IVF [7].
ET-1 is a powerful vasoconstrictor agent and may be implicated in the etiopathogeny of vascular diseases like PIH [8].
In the subgroup of singletons, PIH was significantly higher for OHSS pregnancies than for controls.
The incidence of preterm delivery was higher but with biases of uterine malformation and low BMI.
Other studies have reported a high rate of preterm deliveries: 25 % for Mathur and Jenkins [9] and 44.1 % for Abramov et al. [10].
Bastek et al. recently suggested a link between inflammation, placental dysfunction and preterm births [11].
According to a case control study by Haas J in 2014, rates of preterm delivery were significantly increased among patients with severe OHSS as was the rate of smaller babies. However, this was only in singleton pregnancies [12].
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