classification and treatment of ovarian hyperstimulation syndrome

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07/02/13 Classification and treatment of ovarian hyperstimulation syndrome

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Official reprint from UpToDatewww.uptodate.com

2013 UpToDate

Authors

Vaclav Insler, MD

Bruno Lunenfeld, MD

Section Editors

Robert L Barbieri, MD

William F Crowley, Jr, MD

Deputy Editor

Kathryn A Martin, MD

Classification and treatment of ovarian hyperstimulation syndrome

Disclosures

All topics are updated as new evidence becomes available and our peer review processis complete.

Literature review current through:Jan 2013. | This topic last updated:sep 20, 2011.

INTRODUCTION Most of the problems resulting from gonadotropin therapy for induction of ovulation are related

to the development, luteinization, and ovulation of multiple follicles. (See "Overview of ovulation induction", section

on 'Gonadotropin therapy'.)

The two most serious complications of excessive ovarian stimulation are a high incidence of multiple gestation and

ovarian hyperstimulation syndrome (OHSS):

Multiple gestation is a concern because these pregnancies are associated with increased rates of perinatal

mortality and morbidity. (See "Twin pregnancy: Prenatal issues"and "Triplet pregnancy: Mid and late

pregnancy complications and management".)

OHSS refers to a combination of ovarian enlargement due to multiple ovarian cysts and an acute fluid shift

out of the intravascular space (table 1). It is a potentially life-threatening complication of ovulation induction.

The classification and treatment of established OHSS will be reviewed here. The pathogenesis and prevention of

this disorder are discussed separately. (See "Pathogenesis of ovarian hyperstimulation syndrome"and "Prevention

of ovarian hyperstimulation syndrome".)

CLASSIFICATION AND CLINICAL MANIFESTATIONS Ovarian hyperstimulation is classified into three grades

based upon the severity of symptoms, signs, and laboratory findings [1]. The cardinal event in the genesis of OHSS

is ovarian enlargement with ascites and hypovolemia resulting from an acute fluid shift out of the intravascular

space. (See "Pathogenesis of ovarian hyperstimulation syndrome".)

Grade I ovarian hyperstimulation Grade I (mildhyperstimulation) is characterized by bilateral ovarian

enlargement with multiple follicular and corpus luteum cysts measuring up to 5 by 5 cm. Laboratory findings include

a serum estradiol (E2) concentration greater than 1500 pg/mL (6000 pmol/L) and progesterone concentration

greater than 30 ng/mL (115 nmol/L) in the early part of the luteal phase.

Grade II ovarian hyperstimulation Grade II (moderate hyperstimulation) describes ovaries enlarged up to 12by 12 cm, accompanied by abdominal discomfort and gastrointestinal symptoms (eg, nausea, vomiting, and

diarrhea). A sudden increase in weight of more than 3 kg may be an early sign of moderate hyperstimulation.

Grade III ovarian hyperstimulation Grade III (severe hyperstimulation) is defined by the presence of large

ovarian cysts (more than 12 by 12 cm), ascites, and, in some patients, pleural and/or pericardial effusion,

electrolyte imbalance (hyponatremia, hyperkalemia), hypovolemia, and hypovolemic shock [2-4]. Marked

hemoconcentration, increased blood viscosity, and thromboembolic phenomena, including disseminated

intravascular coagulation, occur in the most severe cases. (See "Pathogenesis and etiology of disseminated

intravascular coagulation".)

Spontaneous regression occurs over 10 to 14 days, but may take longer if implantation occurs.
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Pulmonary manifestations Women with severe OHSS involving the lungs display an extraparenchymal

restrictive type of pulmonary dysfunction due to intraabdominal or pleural fluid accumulation, which limits descent of

the diaphragm and expansion of the lungs. This causes uncoordinated lung ventilation and atelectasis leading to

ventilation-perfusion mismatch and hypoxemia.

Pulmonary infection, thromboembolism, or adult respiratory distress syndrome (ARDS) may further complicate the

clinical picture. As an example, one study of 209 patients with severe OHSS found 4 percent had lobar pneumonia,

2 percent had ARDS, and 2 percent had pulmonary thromboembolism [5]. Clinical manifestations included

dyspnea, tachypnea, moderate hypoxemia, increased alveolar-arterial oxygen difference, hypocarbia, respiratory

alkalosis, and metabolic compensation.

Ascites The degree of ascites is reflected by the woman's weight gain: an initial gain of more than 3 kg

following hCG administration should be considered a warning sign of developing OHSS and warrants close

observation. Women with severe OHSS can gain as much as 15 to 20 kg over 5 to 10 days.

Increased intraabdominal pressure from ascites causes maternal discomfort, which may be severe, and also can

have hemodynamic effects on the maternal circulation (eg, impede renal vein outflow) and can compromise

pulmonary function resulting in hypoxia.

Thromboembolic complications Thromboembolic events are the most serious, but rarest, complications of

OHSS. Thromboses can occur in either the arterial (25 percent) or venous (75 percent) circulations [6,7] and may

lead to permanent neurologic injury or death [8]. The cause of these thromboembolic events is not fully established;

however, it is probably related to hemoconcentration and hypercoagulation and associated with elevated estrogen

concentrations. One study found high levels of factor V, platelets, fibrinogen, profibrinolysin, fibrinolytic inhibitors,

and increased thromboplastin generation in women with OHSS [9]. All of these findings may be regarded as a

result of hemoconcentration and the majority of them are also a consequence of high estrogen levels.

Women with genetic thrombophilia (eg, antithrombin III deficiency, factor V Leiden mutation, protein C or S

deficiency) are most prone to developing thromboembolic events in predisposing situations (eg, use of oral

contraceptive pills, surgery). (See "Overview of the causes of venous thrombosis".)

Some fertility clinics perform screening for thrombophilia before starting ovulation (superovulation) induction therapy

since OHSS is a risk factor for thromboembolic disease. (See "Screening for inherited thrombophilia inasymptomatic populations".)

Thromboembolic complications of OHSS have been reported in the internal jugular, subclavian, axillary, and

mesenteric vessels [5,10]. In one series of five cases of internal jugular vein thrombosis presenting at 7 to 10 weeks

gestation after IVF, two occurred in women who had not had OHSS but had an underlying thrombophilia, while three

occurred in women with severe OHSS and no underlying thrombophilia [11]. (See 'Thromboemboli'below.)

Stroke Thrombotic stroke has been reported in some women with severe OHSS, including three case

reports of middle cerebral artery thrombosis in women who developed hyperstimulation after in vitro fertilization [ 12-

14].

INCIDENCE The incidences of moderate and severe ovarian hyperstimulation compiled from more than 11,300

ovulation induction cycles are 3.1 to 6 percent and 0.25 to 1.8 percent, respectively [1]. In one report, the incidence

of severe OHSS with ovulation induction appeared to be stable over time, while the incidence in the setting of in vitro

fertilization increased from 0.06 percent in 1987 to 0.24 percent in 1999 [15,16]. Sonographic monitoring of ovulation

induction could help to reduce the incidence of OHSS; however, this ability is counterbalanced by the desire to

achieve pregnancy in infertile couples with the fewest number of cycles. In one study, as an example, the

pregnancy rate in hyperstimulated cycles was threefold higher than in nonhyperstimulated cycles [17].

PREGNANCY OUTCOME Inducing mild OHSS appears beneficial for increasing pregnancy rates [17]. Thus,

mild hyperstimulation has been renamed "superovulation" or "controlled ovarian hyperstimulation" to distinguish it

from excessive ovarian stimulation associated with morbid sequelae. Controlled ovarian hyperstimulation is used for
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in vitro fertilization protocols and for treatment of unexplained, cervical, and some forms of male infertility. (See "In

vitro fertilization"and "Overview of infertility".)

However, mild hyperstimulation also raises the incidence of high-order multiple pregnancy (ie, more than two

fetuses), which can result in more spontaneous abortions and perinatal complications. (See "Triplet pregnancy:

Early pregnancy management"and "Triplet pregnancy: Mid and late pregnancy complications and management".)

As an example, one series found superovulation and intrauterine insemination led to twins and triplets-or-more in 20

and 10 percent, respectively, of resulting pregnancies [18]. By comparison, the incidence of twins and triplets in

spontaneously conceived pregnancies is approximately 1/90 and 1/8000, respectively.

Another study reported the frequency of spontaneous abortion was higher among triplets than twins, 25 versus 6

percent [19]. In addition, over 90 percent of triplets have birth weights less than 2500 grams (ie, low birth weight

LBW) and 40 percent are less than 1500 grams (ie, very low birth weight VLBW) [20], whereas the rates of LBW

and VLBW in the general population are approximately 7 and 1.5 percent, respectively [21].

Severe hyperstimulation further worsens pregnancy outcome. This was illustrated in a retrospective review of 163

women with severe OHSS in whom the frequency of singletons, twins, triplets, and quadruplets was 42, 34, 17, and

7 percent, respectively, with a miscarriage rate of 30 percent [ 22].

A controlled study did not show increased feto-maternal morbidity during the second and third trimesters of

gestation among patients who developed OHSS compared to IVF-treated patients without excessive ovarianstimulation [23]. However, uncontrolled studies suggested these pregnancies had a higher rate of gestational

diabetes and pregnancy-associated hypertension [22,24]. More data are needed to better understand whether

OHSS affects the frequency of late pregnancy complications.

TREATMENT The best treatment of OHSS is primary prevention. Preventing ovulation by withholding human

chorionic gonadotropin(hCG) is an effective method of avoiding hyperstimulation in overstimulated ovaries.

Alternatively, aspiration of follicles 36 hours after administration of the ovulatory dose of hCG may lower the risk of

developing clinical hyperstimulation by reducing the mass of luteinized granulosa cells. (See "Prevention of ovarian

hyperstimulation syndrome".)

OHSS is a self-limiting disease; thus, treatment should be symptomatic and conservative. Medical therapy sufficesfor most patients, with laparotomy reserved for catastrophic complications, such as ovarian torsion or rupture and

internal hemorrhage. Women with severe symptoms often require intensive medical care. Vaginal intercourse is

restricted in all grades of OHSS because of the risk of cyst rupture. Patients should also avoid impact-type

activities or strenuous exertion.

Grade I hyperstimulation Treatment is supportive, as needed. However, mild ovarian hyperstimulation can

develop into moderate or severe disease, especially if conception ensues. Therefore, women with mild disease (see

'Grade I ovarian hyperstimulation'above) should be observed for enlarging abdominal girth, acute weight gain, and

abdominal discomfort on an ambulatory basis for at least two weeks or until the appearance of menstrual bleeding.

Grade II hyperstimulation Treatment of moderate hyperstimulation (see 'Grade II ovarian

hyperstimulation'above) consists of observation, bed rest, provision of adequate fluids, and sonographic monitoring

of cyst size. Serum electrolytes, hematocrit, and creatinine should also be evaluated. Some clinicians have

outpatients keep track of their fluid intake and output; intake or output less than 1000 mL/day or a discrepancy in

fluid balance greater than 1000 mL/day would be a cause for concern [2].

Initiation of resolution is apparent when the cysts become smaller on two consecutive ultrasound examinations and

clinical symptoms recede. In contrast, early detection of progression to the severe form of the syndrome is marked

by continuous weight gain (two pounds or more a day), increase in severity of existing symptoms, or the

appearance of new symptoms, such as vomiting, diarrhea, and dyspnea.

Grade III hyperstimulation Medical treatment of severe hyperstimulation (see 'Grade III ovarian
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hyperstimulation'above) is directed toward:

Maintaining blood volume while correcting the disturbed fluid and electrolyte balance

Relieving secondary complications of ascites and hydrothorax

Preventing thromboembolic phenomena

Laboratory tests are listed in the table (table 2) [2]. In addition to frequent monitoring of vital signs and

intake/output, weight and abdominal girth should be checked daily.

Hypovolemia Hypovolemia is caused by extravasation of intravascular fluid ("third-spacing") and isassociated with ascites, hemoconcentration, decreased central venous pressure, low blood pressure, and

tachycardia. Decreased renal perfusion leads to increased reabsorption of sodium and water in the proximal tubule

[25], resulting in oliguria and a low urinary sodium concentration.

Fluid balance should be carefully monitored by net fluid flow (intake/output record), weight and girth measurements,

and hematocrit examinations. A central venous pressure catheter may be required in women who are

hemodynamically unstable. (See "Etiology, clinical manifestations, and diagnosis of volume depletion in adults".)

In general, one to two liters of isotonic fluid is given to such women in the first hour to rapidly restore tissue

perfusion. Further fluids optimally should be given while monitoring the central venous or pulmonary capillary wedge

pressure. Fluid repletion should continue at the initial rapid rate as long as the cardiac filling pressures and the

systemic blood pressure remain low. (See "Maintenance and replacement fluid therapy in adults".)

Plasma expanders such as dextran, human albumin (200 mL of 25 percent albumin over four hours), and plasma

(500 to 1000 mL over 24 hours) supplemented with appropriate electrolytes should be administered early and

repeated as needed. (See "Treatment of severe hypovolemia or hypovolemic shock in adults" .) The effect of this

treatment may be enhanced by the addition of oral indomethacin, which blocks prostaglandin synthesis and

reduces capillary permeability. Hematocrit should be monitored every four hours; plasma expanders can be stopped

when the hematocrit is less than 38 percent [2].

Diuretic agents are not recommended since fluid in the third space is not affected by these drugs. Furthermore,

most diuretics act at the distal tubule with minimal effect on the proximal tubule [26]. Thus, the artificially induced

diuresis may further diminish the intravascular volume, but may be unable to relieve ascites or hydrothorax. Renalfailure may respond to a dopamine drip (0.18 mg/kg per hour) [27]. Oral docarpamine administration could be one of

the options in the management of patients with OHSS requiring dopamine therapy [ 28].

Ovarian enlargement Ovarian cysts associated with grade III OHSS are so large and brittle that surgical

attempts at a palliative procedure usually result in oophorectomy. Therefore, surgery should be avoided unless there

is torsion or cyst rupture with hemorrhage. (See "Oophorectomy and ovarian cystectomy".) Torsion is characterized

by ovarian enlargement, abdominal pain, nausea, progressive leukocytosis, and anemia [ 29]. Treatment may

require oophorectomy, although in many cases the ovary can be saved by unwinding at laparotomy or laparoscopy

[30].

Approach to ascites The degree of ascites is reflected by the woman's weight gain: an initial gain of more

than 3 kg following hCG administration should be considered a warning sign of developing OHSS and warrants

close observation. Women with severe OHSS can gain as much as 15 to 20 kg over 5 to 10 days. (See

'Ascites'above.)

Improvement in creatinine clearance, urine volume, and weight loss in women with severe OHSS treated with

abdominal paracentesis has been described [31,32]. However, other authors have recommended that abdominal

paracentesis for drainage of ascites not be performed because of the danger of intraperitoneal hemorrhage from

inadvertent puncture of the large ovarian cysts [33].

The danger of blind paracentesis has been reduced by using sonographic guidance for the procedure. In our

practice, we have not had a single case of intraperitoneal hemorrhage requiring surgical intervention following
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sonographically guided drainage of ascites in women with severe hyperstimulation syndrome. Paracentesis resulted

in a marked improvement of renal function (due to increased venous return), blood osmolarity, and

hemoconcentration, as well as relief of dyspnea and abdominal discomfort [34].

Another study described 42 cases of severe OHSS treated by transvaginal sonographically guided aspiration of

ascites and intravenous fluid infusion [35]. This treatment relieved symptoms, reduced the hematocrit, improved

renal clearance and urine output, and shortened the duration of hospital stay. Other authors have reinfused the

withdrawn ascitic fluid (after microfiltration) and reported relief of symptoms and improvement of renal function

[36,37].

Pleural effusion As noted, women with severe OHSS involving the lungs display an extraparenchymal

restrictive type of pulmonary dysfunction due to intraabdominal or pleural fluid accumulation, which limits descent of

the diaphragm and expansion of the lungs [5]. (See 'Pulmonary manifestations'above.) Pleural effusions should be

drained to relieve dyspnea. Paracentesis may also be useful in alleviating breathing difficulties in patients with

ascites and hydrothorax [38].

Thromboemboli Thromboembolic events are the most serious, but rarest, complications of OHSS.

Thromboses can occur in either the arterial (25 percent) or venous (75 percent) circulations [6,7] and may lead to

permanent neurologic injury or death [8].

Prophylactic anticoagulation with heparin or low molecular weight heparin, antiembolism stockings, and or

intermittent pneumatic compression boots should be considered to minimize the risk of venous thrombosis [2].

Treatment of thromboembolic complications is anticoagulation with heparin. (See "Therapeutic use of heparin and

low molecular weight heparin".)

Resolution After a period of several days, third space fluid begins to re-enter the intravascular space,

hemoconcentration reverses, and natural diuresis ensues. The patient feels better and her appetite and ability to

take oral fluids improve. Intravenous fluids are tapered as oral intake increases. Some clinicians limit oral intake to

1000 mL/day at this time to facilitate diuresis and maintain euvolemia [2]. Complete resolution typically takes 10 to

14 days from the onset of initial symptoms.

SUMMARY Carefully maintaining blood volume, correcting electrolyte imbalance, and relieving secondary

complications of ascites and hydrothorax are generally sufficient for supporting the patient during the severe phaseof ovarian hyperstimulation. Anticoagulant therapy is usually unnecessary if these therapies are promptly

employed. Blood coagulation may be monitored because of the danger of disseminated intravascular clotting.

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GRAPHICS

Clinical findings in women with ovarian hyperstimulation syndrome

Bloating

Nausea, vomiting, diarrhea

Lethargy

Shortness of breath

Oliguria

Rapid weight gain

Hemoconcentration

Leukocytosis

Hyponatremia, hyperkalemia

Pleural and pericardial effusions

Ascites

Hypercoagulability and thrombosis

Adult respiratory distress syndrome


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Laboratory monitoring in women with grade 3 OHSS

Daily

Leukocyte count

Hemoglobin and hematocrit

Electrolytes

Once, repeat as indicated

Liver function tests

Prothrombin and partial thromboplastin time

Chest radiograph (if respiratory symptoms are present)

classification and treatment of ovarian hyperstimulation syndrome

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