Case Report

ovarian hyperstimulation syndrome: an important complication of in vitro fertilization

Abstract

Ovarian hyperstimulation syndrome is an iatrogenic complication of ovarian stimulation for assisted reproduction techniques (Budev M, Arroliga A, Falcone T. Ovarian hyperstimulation syndrome. Crit Care Med 2005; 33(10) Supplement: S301-S306; Beerendonk CCM, van Dop PA, Braat DDM, Merkus JMWM: Ovarian hyperstimulation syndrome: facts and fallacies. Obstet Gynecol 1998; 53 (7):439-449). The syndrome is characterized by cystic enlargement of the ovaries and fluid shifts from the intravascular to the third space (Beerendonk CCM, van Dop PA, Braat DDM, Merkus JMWM: Ovarian hypersti- mulation syndrome: facts and fallacies. Obstet Gynecol 1998; 53(7):439-449). We present a patient with a classic presentation of severe ovarian hyperstimulation syndrome.

A 31-year-old woman presented to the emergency department with a several-day history of increasing abdom- inal pain, swelling, and dyspnea. She had undergone assisted reproduction technique 6 days before. She admitted to nausea, but no vomiting. She denied chest pain, cough, or Vaginal bleeding.

Physical examination revealed a well-nourished, well- developed female in mild distress. Vital signs were the following: temperature, 96.1?F; pulse, 42 beats/min; respiratory rate, 20; and blood pressure, 56/43 mm Hg. The patient’s heart rate was noted to be bradycardic, but with a regular rhythm and without murmur, rub, or gallop. The lungs were clear to auscultation. The abdomen was distended and diffusely tender with voluntary guarding and shifting dullness. There was no rebound. Bowel sounds were present but hypoactive. The pelvic examina- tion was deferred.

The patient was placed on cardiac and Pulse oximetry monitors, given oxygen via nasal cannula and a 1-L normal saline bolus. The serum white blood cell count was markedly elevated at 21.6 x 10³/uL with 81% polys, 14% lymph, and 4% monos. The hemoglobin was 16.6 g/dL, hematocrit 47.7%, and platelet count normal. Glucose, serum urea nitrogen, creatinine, and electrolytes were all within normal

limits. The serum pregnancy test was positive and a portable Chest x-ray was normal.

After intravenous (IV) fluid administration, the blood pressure had increased to 117/82 mm Hg and the pulse rate to 74 beats/min. The in vitro fertilization fellow evaluated the patient and ordered 500 mL of 5% albumin intravenously and 5000 U of heparin subcutaneously. Pelvic ultrasound revealed a large amount of ascites and enlarged ovaries bilaterally. The fellow performed an ultrasound-guided intravaginal culdocentesis, removing 1600 mL of fluid, with significant relief of the patient’s abdominal pain. The patient was admitted to the hospital with the diagnosis of Ovarian hyperstimulation syndrome .

Ovarian hyperstimulation syndrome is a known compli- cation of ovarian stimulation.

There have been multiple classification systems developed over the years, most recently by Rizk and Aboulghar [1]. They reclassified the syndrome into moderate and severe. Moderate OHSS is defined as pain, nausea, abdominal distension, no clinical evidence of ascites, and normal hematological and biochemical profiles. Severe OHSS was subcategorized into grades A, B, and C. Grade A includes dyspnea, oliguria, nausea, vomiting, diarrhea, and abdominal pain; clinical evidence of ascites, plus marked distension of the abdomen or hydrothorax; Sonographic findings of large ovaries and marked ascites; and a normal biochemical profile [1]. Grade B includes all of the symptoms of grade A, plus massive tension ascites, markedly enlarged ovaries, severe dyspnea, marked oliguria, and biochemical changes. For grade C, the OHSS must be complicated by respiratory distress syndrome, renal failure, or venous thrombosis [1].

The pathogenesis of OHSS involves increased vascular permeability that leads to fluid shifts from the intravascular to the interstitial space [2]. The ovaries increase in size and produce vasoactive substances that increase capillary permeability. This increased vascular permeability results in increased fluid shift out of the intravascular space and into the third space. As this extravascular protein-rich exudate accumulates in the peritoneum, there are associated intra- vascular Volume depletion, hemoconcentration, and hypoal- buminemia [3]. These changes in turn can cause hypotension and tachycardia. The subsequent decreased renal perfusion induces resorption of sodium and water, which results in oliguria and sodium retention [3].

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115.e4 Case Report

The clinical presentation of OHSS varies considerably. The degree of ascites can range from mild to tense. The ascites leads to Abdominal distention and pain. Nausea, vomiting, and diarrhea occur secondary to intestinal edema and associated paralytic ileus. Dyspnea and tachypnea are common, secondary to elevation of the diaphragm, development of Pleural effusions, and interstitial edema [2]. Patients may present with signs and symptoms of thromboembolism, including thrombophlebitis and pul- monary embolism.

The workup of a patient with suspected moderate or severe OHSS should include complete blood count; basic metabolic profile including serum urea nitrogen, creatinine, and glucose; quantitative ?-human chorionic gonadotropin; and liver function tests and Coagulation studies [4]. electrolyte abnormalities, especially hyponatremia and hyperkalemia, are common [3]. A hematocrit greater than 45%, an elevated serum creatinine, and abnormal liver function studies all indicate severe OHSS [5]. Leukocytosis and thrombocytosis are common. Ultrasound should be considered to evaluate the extent of ovarian enlargement and the presence/degree of pelvic and abdominal fluid accumula- tion, as well as evidence of Ovarian torsion, hemorrhage, or Ectopic pregnancy. Patients with respiratory symptoms should have pulse oximetry and a CXR. Evaluation for deep venous thrombosis or pulmonary embolism is indicated as suggested by history or physical examination.

In general, mild OHSS does not require any specific treatment; most symptoms will resolve within 1 week. The patient should have close follow-up and be instructed to seek attention if the symptoms worsen. Most patients with moderate OHSS can also be managed as an outpatient. For patients with significant vomiting, intra- venously administered crystalloids and antiemetics may be necessary. discharge instructions should include oral hydration and self-monitoring for urine output and weight gain [4].

Severe OHSS must be treated aggressively. These patients should be placed on a cardiac monitor, administered oxygen, and volume replacement with intravenously administered normal saline. Pelvic examination should be deferred to prevent rupture of enlarged ovaries and subsequent hemor- rhage [6]. The use of colloids, such as albumin, is controversial. Diuretics play no role [3]. Ultrasound-guided paracentesis, from either an abdominal or intravaginal approach, has been shown to result in improvement in

dyspnea, increase in diuresis, and decrease in abdominal discomfort and hematocrit [3]. The role of prophylactic heparin administration is unclear. Some experts recommend heparin prophylaxis (ie, 5000 U BID subcutaneously) to all patients who are hospitalized for OHSS, whereas others recommend restricting its use to patients with hemoconcen- tration [3,7].

Ovarian hyperstimulation syndrome should be considered in any woman undergoing assisted reproduction technique that presents with abdominal pain or dyspnea. Evaluation and management of patients with the Severe form of OHSS includes IV crystalloid fluid resuscitation, bedside ultrasound, and early consultation with the patient’s infertility specialist.

Heather M. Justice MD Francis L. Counselman MD Department of Emergency Medicine Eastern Virginia Medical School and Emergency Physicians of Tidewater

Norfolk, VA 23507, USA E-mail address: [email protected]

doi:10.1016/j.ajem.2007.06.031

References

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2. Vlahos NF, Gregoriou O, Part VI. Assisted reproduction prevention and management of ovarian hyperstimulation syndrome. Ann N Y Acad Sci 2006;1092:247-64.
3. Delvigne A, Rozenberg S. Review of clinical course and treatment of ovarian hyperstimulation syndrome (OHSS). Hum Reprod Update 2003;9(1):77-96.
4. Rutkowski A, Dubinsky I. Ovarian hyperstimulation syndrome: imperatives for the emergency physician. J Emerg Med 1999;17(4): 669-72.
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