Number and size of follicles during ovarian stimulation

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Chapter 36: Prediction and management of OHSS

Table 36.1. Classiﬁcations of ovarian hyperstimulation syndrome (1967–1999)

Study Mild Moderate Severe

Rabau et al. [1] Grade 1: estrogen >150 μg and

Schenker and

Weinstein [2]

Golan et al. [3] Grade 1: abdominal distension

Navot et al. [4] Severe OHSS: variable enlarged

Rizk and

Aboulghar [15]

pregnanediol >10 mg/24 h

Grade 2: + enlarged ovaries and

possibly palpable cysts Grade 1 and 2 were not included under the title of mild OHSS

Grade1:estrogen

>150 μg/24 h and pregnanediol >10 mg/24 h

Grade 2:grade 1+ enlarged

ovaries, sometimes small cysts

and discomfort

Grade 2: grade 1 + nausea,

vomiting, and/or diarrhea, enlarged ovaries 5–12 cm

Discomfort, pain, nausea,

abdominal distension, ultrasonic evidence of ascites and enlarged ovaries; normal hematological and biological proﬁles

Grade 3: grade 2 + conﬁrmed

palpable cysts and distended abdomen

Grade 4: grade 3 + vomiting and

possibly diarrhea

Grade 3: grade 2+ abdominal

distension

Grade 4: grade 3 + nausea, vomiting

and/or diarrhea

Grade 3: grade 2 + ultrasound

evidence of ascites

Grade A: dyspnea, oliguria, nausea,

vomiting, diarrhea, abdominal pain, clinical evidence of ascites, marked distension of abdomen or hydrothorax; US showing large ovaries and marked ascites; normal biochemical proﬁle

Grade 5: grade 4 + ascites and

possibly hydrothorax

Grade 5: grade 4 + large ovarian

cysts, ascites and/or hydrothorax

Grade 4: grade 3 + clinical

evidence of ascites and/or hydrothorax and breathing diﬃculties

ovary; massive ascites ± hydrothorax; Hct >45%; WBC >15 000; oliguria; creatinine

1.0–1.5; creatinine clearance ≥50ml/min; liver dysfunction; anasarca

Grade B: Grade A plus massive

tension ascites, markedly enlarged ovaries, severe dyspnea and marked oliguria, increased hematocrit, elevated serum creatinine and liver dysfunction

Grade 6: grade 5 +

changes in blood volume, viscosity, and coagulation time

Grade 6: marked

hemoconcentration + increased blood viscosity, and possibly coagulation abnormalities

Grade 5: grade 4 +

hemoconcentration, increased blood viscosity, coagulation abnormality, and diminished renal perfusion

Critical OHSS: variably

enlarged ovary; tense ascites ± hydrothorax; Hct >55%; WBC ≥25 000; oliguria; creatinine ≥1.6; creatinine clearance <50 ml/min; renal failure; thromboembolic phenomena; ARDS

Grade C: Complications as

respiratory distress syndrome, renal shutdown,

or venous

thrombosis

Reproduced with permission from Aboulghar and Mansour [14].

There was a signiﬁcant correlation between the baseline ovarianvolumeandthesubsequentoccurrenceofOHSS.The authors suggested that volumetry of the ovaries could help to detect patients at risk.

Lass et al. [24] studied whether ovarian volume in the early follicular phase of WHO group II anovulatory patients would predict the response to ovulation induction with gonadotropins. They analyzed retrospective data from two prospective randomized multicenter studies, in cluding 465 patients undergoing ovulation induction, and found that WHO Group II anovulatory women with medium-sized or large ovaries undergoing low-dose gonadotropin stimulation for ovulation induction have a higher risk for OHSS than women wi th small ov aries.

Number and size of follicles during ovarian stimulation

Ultrasound is widely used for monitoring follicular development in assisted conception [25,26]. The number, size, and

pattern of distribution of the follicles are important in the prediction of OHSS. Tal et al. found a positive correlation between the mean number of immature follicles and OHSS [27]. One of the most often quoted articles in reference to the prediction is that by Blankstein et al. (1987), who stated that a decrease in the fraction of the mature follicles and an increase in the fraction of the very small follicles correlated with an augmented risk for the development of severe OHSS [28]. More recently, Kwee et al. found that women with an antral follicle count of 15 or more are at a higher risk of developing OHSS (Table 36.3)[29].

Low intravascular ovarian resistance

Moohan et al. [30] assessed the intraovarian blood ﬂow in relation to the severity of OHSS in 30 patients with OHSS after embryo transfer who also had sonographic evidence of ascites. The authors measured the resistance to blood ﬂow within the ovaries of 11 patients with severe OHSS and 19 patients with mild OHSS using transabdominal

303

/ hCG/

ecept

Section 4: Early pregnancy after infertility treatment

Table 36.2. Prediction of OHSS

History and physical

1. OHSS in a previous cycle

2. Polycystic syndrome

3. Young patient

4. Low body mass index

5. Hyperinsulinism

6. Allergies

During ovarian stimulation

1. High serum estradiol, rapid slope of E

2. Ultrasonography

a. Baseline PCO pattern b. PCO pattern of response to GnRH before gonadotropins c. Large number of follicles, >20, in each ovary

3. Doppler: low intraovarian vascular resistance

Outcome of ART cycles

1. Conception cycles

2. Multiple pregnancy

, and absolute value

PIGF VEGF

Binding domain

Dimerization domain

Split tyrosine kinase domain

121 145 165

VEGFB

121

145

165

VEGFC

S S

VEGFD

hCG

LH / hCG

receptor

VEGF

Fluid

extravasation

AscitesHydrothorax Anasarca

hCG

LH / hCG receptor

LH / hCG

receptor

VEGER-1

(Flt-1)

Figure 36.9. Vascular endothelial growth factor receptors.

R2-VEGF

Disrupts

tight junctions

Edema

Figure 36.10. Vascular endothelial growth factor receptors and vascular

permeability.

VEGER-2

(Flk-1)

VEGF

Physiologic conditions

Increases i (Ca2+)

INCREASES

PERMEABILITY

VEGER-3

(Flt-4)

R1-VEGF

Maintains

intracellular

assembly

Avoids plasma

leakage

ultrasonography with color ﬂow and pulsed Doppler imaging. The pulsatility index (PI), the resistance index (RI), and the S-D ratio, all measures of downstream vascular impedance, were signiﬁcantly lower in severe OHSS patients. More than two-

Figure 36.8a,b. Pathophysiology of ovarian hyperstimulation syndrome.

thirds of the patients with RI <0.48 had pleural eﬀusion. In patients with either PI <0.75 or S-D <1.92, pleural eﬀusion was observed in more than one-half. The blood ﬂow velocity did not diﬀer signiﬁcantly between the two groups despite the fact that

304

(a) (b)

Figure 36.11a,b. Polycystic ovaries at the beginning of an IVF cycle.

Chapter 36: Prediction and management of OHSS

Figure 36.12. Color Doppler ultrasound image of a polycystic ovary indicating

active blood ﬂow. Reproduced with permission from reference [49].

(a)

Mean ovarian stromal blood flow (cm/s)

Figure 36.13. Increased ovarian stromal blood ﬂ ow in PCOS. Reproduced with

permission from reference [ 50], ﬁ gure 5– 4

(b)

max

Control

PCO PCOS

Figure 36.14a,b. Increased ovarian blood ﬂow by Doppler in severe ovarian hyperstimulation syndrome.

305

Section 4: Early pregnancy after infertility treatment

Table 36.3. Antral follicle count and prediction of OHSS

Total AFC Sensitivity Speciﬁcity PPV Accuracy

<10 0.94 0.71 0.36 0.76

<12 0.88 0.80 0.44 0.81

<14 0.82 0.89 0.58 0.88

<16 0.47 0.96 0.67 0.88

<18 0.29 0.98 0.71 0.87

Reproduced with permission from Kwee. et al. [29]. PPV = positive predictive value.

Table 36.4. Primary prevention of OHSS

The ten commandments

1. Prediction of OHSS from history, examination, and ultrasound

2. Laparoscopic ovarian drilling in PCOS patients

3. Metformin in PCOS patients

4. Octreotide in PCOS patients

5. Low-dose gonadotropins in PCOS patients

6. GnRH antagonist protocol

7. Recombinant LH to trigger ovulation

8. GnRH agonist to trigger ovulation’

9. In-vitro maturation of oocytes

10. Replacement of only one embryo

Reproduced with permission from Rizk [6].

Table 36.5. Secondary prevention of OHSS

The ten commandments

1. Withholding hCG +/– continuation of GnRH-a/GnRH antagonist

2. Coasting or delaying hCG: currently most popular method

3. Use of GnRH-a to trigger ovulation

4. Follicular aspiration

5. Progesterone for luteal phase

6. Cryopreservation and replacement of frozen-thawed embryos at a

subsequent cycle

7. Dopamine agonist

8. Albumin, administration at time of retrieval

9. Glucocorticoid administration

10. Aromatase inhibitors

Reproduced with permission from Rizk [6].

Figure 36.15. Ascites in moderate ovarian hyperstimulation syndrome in early

pregnancy.

Figure 36.16. Twins associated with ovarian hyperstimulation syndrome.

there were changes in vascular impedance. A close correlation was observed between the OHSS severity and the intraovarian blood ﬂow resistance. The authors suggested that measurements of intraovarian vascular resistance in patients undergoing controlled ovarian hyperstimulation may help in predicting those patients at particular risk of developing OHSS.

The combination of estradiol and ultrasonograp hy oﬀers the best chance for the prediction of OHSS. Ultrasonographic follow-up of the leading follicles should be used for the determination of the hCG administration and serum estradiol measurement, and sonographic visualization of small and intermediate follicles should be used to determine the likelihood of OHSS.

Prevention of OHSS

Rizk in 1993 suggested the “Ten Commandments” for the prevention of OHSS [31]. Today the list has expanded to two lists of “Ten Commandments” [32]. The ﬁrst list addresses the primary prevention of OHSS, which includes options before stimulation such as ovarian diathermy, and during stimulation such as the use of low-dosage gonadotropins [32](Table 36.4). The second list addresses the secondary prevention of OHSS, which includes withholding or delaying hCG, use of luteinizing hormone or gonadotropin-releasing hormone (GnRH) agonist (GnRh-a) in place of hCG for triggering ovulation, and progesterone for luteal phase support (Figure 36.17; Table 36.5).

Rizk has recently noted that among the options available for the prevention of OHSS, “coasting”, or delaying hCG administration until the estradiol levels drop to below 3000 pg/ml, is currently the most popular method [26]. When estradiol levels increase rapidly in women undergoing controlled ovarian hyperstimulation (COH) with the concomitant administration of gonadotropins and GnRH-a, if gonadotropins and not

306

Chapter 36: Prediction and management of OHSS

Coasting

GnRH-a

FSH r/ hMG

5000 Ul hCG

Menses

22 days

RESULTS

hCG

Endothelium granulosa

Figure 36.18. VEGF receptor blockade in prevention of ovarian

hyperstimulation syndrome.

SU-5416

VEGF-R2VEGF-R2

RESULTS

VEGF

R2-VEGF

E >4000 pg/ml

OVARIAN

ASCULAR

PERMEABILITY

>18mm

hCG

GnRH-a are withheld, as there is no endogenous gonadotropin secretion to sustain follicular growth, a rapid decline in estradiol levels will occur (Figure 36.17). Healthy developing follicles tolerate a brief period of gonadotropin deprivation, but granulosa cells of smaller follicles are less tolerant of withholding of gonadotropin stimulus [33,34,35]. Further evidence that could explain the coasting physiology is that VEGF expression and secretion are signiﬁcantly decreased in coasted patients [33]. This is the rationale for coasting to reduce the risk/severity of OHSS in a high-risk population [33,34,35].

In women who develop OHSS, VEGF is overexpressed and produced by granulosa-lutein cells and released into the follicular ﬂuid in response to hCG, inducing increased capillary permeability. hCG induces the expression of VEGF in cultured granulosa-lutein cells of women developing OHSS [16]. Similarly, hCG stimulates the release of VEGF in human endothelial cells, which in turn act in an autocrine manner, increasing vascular permeability (VP). Thus, both the granulosa and endothelial cells may be involved in the production and release

Figure 36.17. Coasting for prevention of ovarian

hyperstimulation syndrome.

36–38 h

of VEGF in women who develop OHSS, although the concept that granulosa-lutein cells behave as actual endothelial cells has also been proposed [33,34,35]. The ability to reverse hCG action on VP by targeting the VEGF-R2 employing SU5416 was not only reassuring of the key role of VEGF in OHSS but also provided new insights into the development of strategies to prevent and treat the syndrome based on its pathophysiological mechanism [36], rather than using empirical approaches as we do today (Figures 36.18, 36.19, 36.20).

Dopamine receptor 2 agonists inhibit VEGF-R2-dependent VP and angiogenesis when administered at high doses in animal cancer models. To test whether VEGF-R2-dependent VP and angiogenesis could be segregated in a dose-dependent fashion with cabergoline, a well-established OHSS rat model supplemented with prolactin was used [37]. Low-dose cabergoline at 100 μg/kg reversed VEGF-R2-dependent VP without aﬀecting luteal angiogenesis through partial inhibition of ovarian VEGF-R2 phosphorylation levels. No luteolytic eﬀects (serum progesterone levels and luteal apoptosis unaﬀected) were observed. Cabergoline administration also did not aﬀect VEGF/VEGF-R2 ovarian mRNA levels (Figures 36.18, 36.19,

36.20)[37,38,39,40]. In a recent prospective, randomized, con-

trolled trial, Carizza et al. found that, in humans, cabergoline was beneﬁcial in the prevention of early-onset but not late-onset OHSS [41]. The authors studied 166 patients with estradiol concentrations of greater than 4000 pg/ml on the day of hCG administration. They all received 20 g of intravenous human albumin on the day of oocyte retrieval. The patients were randomized into two groups: group A (n =83)received0.5mg. oral cabergoline per day for 3 weeks beginning on the day after oocyte retrieval, and group B (n = 83) received no medication. In group A, no patients progressed to early OHSS and 9 patients develop

ed late OHSS. In group B, 12 patients progressed to early OHSS and 3 to late OHSS. The authors concluded that cabergoline decreased the risk of early OHSS signiﬁcantly (P < 0.001), but not late-onset OHSS.

307

Section 4: Early pregnancy after infertility treatment

Cabergoline and OHSS prevention

Figure 36.19. Cabergoline and prevention of

ovarian hyperstimulation syndrome.

• Oocyte donors

• GnRHa

• Hemogram

• Creatinine

• Na

, K

• GOT, GPT

• Prolactin

VEGF

VEGF-R2

HCG

• >20–30 fol. >12 mm

• >20 retrived oocytes

• Randomization

• Cb2 0,5 mg/day or placebo during 8 days

6420

Days

• Clinical evaluation

• Vaginal ultrasound

• Laboratory

Figure 36.20. Molecular mechanism of dopamine

agonist on vascular permeability.

Dopamine

receptor

Dopamine

Treatment of OHSS

The management of OHSS depends on the severity and the presence or absence of complications [42]. Most patients with mild or moderate OHSS are treated as outpatients. The comfort of the physician and the reliability of the patient are crucial determinants. Patients with severe OHSS (grade C) are treated in the hospital, while patients with grades A and B may be treated in the IVF unit or the hospital depending on the presence or absence of complications. The indications for hospitalization are listed in Table 36.6.

Outer

cell

Inner

cell

Medical treatment in the hospital consists of correction of circulatory volume and electrolyte imbalance (Figure 36.21). Anticoagulation is given in patients who have developed thromboembolism or to those who are at risk of developing thromboembolism. Today, we have a more liberal approach to anticoagulating these patients. Diuretics should not be administered in patients with severe OHSS, except for the treatment of pulmonary edema. Navot and colleagues have the largest experience of the management of patients with severe OHSS using albumin and Lasix, and their experience should be consulted in the management of these critical patients [4].

308

Chapter 36: Prediction and management of OHSS

Ultrasonography is also essential in the management of severe OHSS. Rizk and Aboulghar in 1991 recommended that aspiration of ascitic ﬂuid be performed transvaginally or transabdominally under ultrasonographic guidance in the presence of tense ascites [42]. Aboulghar et al. demonstrated that transvaginal aspiration improves patients’ symptoms and renal function (43]. The increased intra-abdominal pressure may compromise venous return and, consequently, cardiac output as well as threaten renal edema and possibly thrombosis. In the presence of tense ascites and oliguria, increasing levels of creatinine, or hemoconcentration that is unresponsive to medical therapy, ultrasound-guided aspiration of ascitic ﬂuid must be performed. The dramatic improvement in clinical symptoms (rise in urine output and creatinine clearance, decrease in hematocrit, alleviation of dyspnea and abdominal discomfort) supports this treatment modality as safe and exceptionally beneﬁcial [44]. Repeated transabdominal aspiration can also be safely performed [45]. Chen et al. investigated the eﬀects of paracentesis on uterine and intraovarian hemodynamics by color Doppler ultrasound to determine the inﬂuence of

Table 36.6. Indications for hospitalization of patients with severe OHSS

1. Severe abdominal pain or peritoneal signs

2. Intractable nausea and vomiting that prevents ingestion of food and

adequate ﬂuids

3. Severe oliguria or anuria

4. Tense ascites

5. Dyspnea or tachypnea

6. Hypotension (relative to baseline), dizziness, or syncope

7. Severe electrolyte imbalance (hypernatremia, hyperkalemia)

Reproduced with permission from Rizk [6].

repeated paracentesis on pregnancy outcome in severe OHSS [45]. In their study, 41 abdominal paracenteses were performed on 7 pregnant women with tense ascites, and thoracocenteses were performed on 3 pregnant women with pleural eﬀusion. Pulsatility index and maximum peak systolic veloc ity of uterine and intraovarian arteries were measured before and after each intervention. The mean pulsatility index of uterine arteries was decreased signiﬁcantly after paracentesis but not after thoracocentesis. Interestingly, the authors observed a decrease in the uterine pulsatility index in 13 out of 14 paracenteses (93%) with less than 2500 ml of ascites removed compared with 8 out of 13 (62%) with more than 2500 ml of ascites removed. After paracentesis, there were no signiﬁcant changes in the intraovarian pulsatility index and mean peak systolic velocity in either group. The authors observed no diﬀerence in miscarriage rates between the two groups and concluded that repeated abdominal paracentesis increased uterine perfusion without adverse eﬀects on pregnancy outcome in patients with severe OHSS [43]. Al-Ramahi et al. reported three cases where an indwelling peritoneal catheter was used to decrease the need for paracentesis. Under ultrasound guidance, a closed-system Dawson–Mueller catheter with “simp-loc” locking design was inserted to allow continuous drainage of the ascitic ﬂuid [46]. The authors concluded that continuous drainage of the ascitic ﬂuid is preferable to multiple abdominal paracenteses in the management of severe OHSS. Abuzeid et al. studied the eﬃ cacy and safety of percutaneous pigtail catheter drainage for the management of ascites complicating severe OHSS [47]. A pigtail catheter was inserted under ultrasound guidance and kept in place until drainage ceased. Surgery should be avoided in most patients with OHSS, except in the cases of ovarian torsion or hemorrhage.

Management

Admission for monitoring

1. Strict fluid chart

2. Plasma and urine osmolarity

3. Urea and electrolytes

4. Clotting parameters

5. Liver function tests

6. Pregnancy test

7. Pelvic sonography

8. Invasive hemodynamic monitoring

Medical treatment

1. Correction of circulatory and electrolyte imbalance

• correction of electrolyte imbalance

• plasma expanders

2. Anticoagulants: clinical or laboratory evidence of thromboembolism

3. Prostaglandin synthetase inhibitors could be hazardous to renal perfusion

4. Antihistamines: not effective

5. Danazol: not effective

6. Diuretics: deplete intravascular volume

7. Dopamine: in oliguric patients

1. Moderate OHSS

2. Severe OHSS:

conservative treatment and follow-up

Surgical treatment

Laparotomy

1. Experienced surgeon

2. Only if hemorrhage

• torsion

• rupture

• ectopic

3. Only hemostatic

Laparoscopy Unwinding of twisted ovarian cyst

Aspiration of ascitic fluid

1. Abdominal paracentesis

2. Transvaginal aspiration

Advantages:

1. Improves symptoms

2. Improves renal function and urine output

3. Shortens venous return and cardiac output

4. Improves venous return and cardiac output

Precautions:

1. Sonographic guidance

2. Replacement of plasma protein

3. Repeat aspiration may be required

Figure 36.21. Management of ovarian

hyperstimulation syndrome.

309

Section 4: Early pregnancy after infertility treatment

Key points in clinical practice

Ovarian hyperstimulation syndrome is characterized by

bilateral cystic ovarian enlargement and third-space ﬂuid

shift resulting in ascites and pleural eﬀusion.

Severe ovarian hyperstimulation syndrome might be

associated with serious complications such as

thromboembolism, adult respiratory distress syndrome,

and kidney failure.

Human chorionic gonadotropin increases VEGF

production by granulosa cells and endothelial cells, which

results in increased vascular permeability.

The cornerstone of successful prevention of OHSS is

accurate prediction.

Previous history of OHSS or polycystic ovary syndrome is

highly predictive of the development of OHSS during

ovarian stimulation.

Ultrasound is essential for the prediction of OHSS before,

during, and after the treatment cycle.

Baseline antral follicle count and ovarian volume are

strongly associated with OHSS.

The presence of a large number of follicles (>20 per ovary)

and increase in the small and intermediate follicles are

associated with an increased risk for the development of

severe OHSS.

Increased intraovarian blood ﬂow and low intravascular

ovarian resistance are correlated with the severity of OHSS

in patients who develop the syndrome.

The presence of multiple pregnancy increases the risk of the

severity and duration of OHSS.

The primary prevention of OHSS can be achieved by the use

of low-dose gonadotropins and, in some cases, ovarian

drilling prior to IVF.

The secondary prevention of OHSS involves delaying the

hCG, known as “coasting,” and, in some cases, cancellation

of the hCG.

The medical treatment of OHSS consists of

correction of circulatory volume and electrolyte

imbalance.

Ultrasonographic guidance of transvaginal or

transabdominal aspiration of ascites improves the

symptoms of patients with OHSS.

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