Article, Gynecology

An unusual cause of tachycardia, hypotension, and intraabdominal free fluid: ovarian hyperstimulation syndrome

Case Report

An unusual cause of tachycardia, hypotension, and

?intraabdominal free fluid: ovarian hyperstimulation syndrome?

Abstract

We report a case of Ovarian hyperstimulation syndrome in a 37-year-old female who had recently under- went assisted reproductive technology involving oocyte retrieval. Her emergency department (ED) presentation, clinical course, and a discussion of ovarian hyperstimulation syndrome are also presented. Ovarian hyperstimulation syndrome is a critical diagnosis in emergency medicine, and emergency physicians must consider it in the differential for any female nontrauma patient presenting with hypoten- sion, tachycardia, and abdominal pain.

A 37-year-old female presented to the ED 24 hours after undergoing oocyte retrieval that was significant for ovarian hyperstimulation evidenced by collection of greater than 50 follicles and estrogen level greater than 15 000 pmol/L. She complained of severe weakness, light-headedness, and sweating. She also noted abdominal pain but denied vaginal discharge, nausea, and vomiting. She was a previously healthy female with medical history significant only for Polycystic ovarian syndrome, infertility, and gastroesopha- geal reflux disease for which she was taking prenatal vitamins, ranitidine, colace, and roxicet. The day before presentation, she underwent oocyte retrieval after ovarian hyperstimulation treatment with follitropin ?, recombinant human chorionic gonadotropin ?, and leuprolide acetate. She felt fine immediately after her procedure but developed mild symptoms of sweating, abdominal pain, and bloating within 8 hours of the procedure.

On examination, the patient had a blood pressure of 85/40 mm Hg, a pulse rate of 160 beats per minute, a respiratory rate of 32 per minute, and was afebrile. She was in acute distress with diaphoresis, shortness of breath, abdominal pain, mildly altered mental status, and an electrocardiogram consistent with sinus tachycardia. The result of her physical examination was also notable for lower abdominal tender-

? Acknowledgements and Disclaimers: This work has not been published elsewhere. It will not be submitted elsewhere while under consideration by the American Journal of Emergency Medicine.

ness without rebound or guarding and a bedside emergency medicine ultrasound demonstrating a large amount of free fluid in the abdomen and pelvis with a 2-cm stripe at Morrison’s pouch and bilateral ovaries with multiple cysts. The patient was given 2 L of normal saline intravenously more than 30 minutes in the ED, and her pulse rate was subsequently reduced to 90 beats per minute and a blood pressure of 105/50 mm Hg by the time she left the ED. During her hospital stay, she was treated with intravenous hydration, paracentesis done twice along with diuresis, and albumin therapy for residual ascites and mild Pleural effusions. The patient responded well to these therapies and was discharged on hospital day 12.

Ovarian hyperstimulation syndrome is an uncommon ED diagnosis, occurring in 0.2% to 1% of all stimulation cycles in assisted reproduction [1]. The proliferation of assisted reproduction technology makes it increasingly likely that emergency physicians may encounter patients having OHSS of varying clinical severity. Patients with OHSS may present to the ED with a myriad of chief complaints, but the diagnosis must be considered in the evaluation of any female presenting to the ED with hypotension, tachycardia, and/or an ultrasonic Abdominal examination result positive for free fluid. Although the cause of OHSS has not been completely elucidated, it is believed that increased capillary permeability plays a major role in this syndrome. Human chorionic gonadotropin-mediated ovarian release of factors involved in

Fig. 1 Pelvic ultrasound in ovarian hyperstimulation syndrome patient demonstrating enlarged ovaries with multiple large corpus luteal cysts and fluid in the pelvis.

0735-6757/$ – see front matter.

736.e4 Case Report

Fig. 2 Left ovary of patient with ovarian hyperstimulation syndrome demonstrating enlargement with multiple luteal cysts.

the renin-angiotensin system, cytokines including the interleukins, tumor necrosis factor, and vascular endothelial growth factor among others are thought to be involved in initiating the cascade of symptoms in OHSS [1,2]. The usual presenting signs and symptoms include those resulting from excessive fluid “leakage” including ascites, edema, and hypovolemia. Abdominal/pelvic ultrasound result will likely demonstrate fluid in the abdomen, multiple corpus lutea on both ovaries, and fluid within the pelvis (see Figs. 1 and 2). Serious complications of this syndrome may include thromboembolism, systemic inflammatory response syn- drome, adult respiratory distress syndrome, or even death. Researchers have sought clinical and demographic predictors to help identify those at highest risk for this syndrome. Although it is still not possible to predict the development of OHSS, it appears that increased estradiol levels and the collection of larger numbers of oocytes during assisted reproduction technology increase the likelihood of OHSS [3]. Techniques to lessen the incidence of Severe OHSS have involved the use of gonadotropin-releasing hormone (GnRH) agonists to induce oocyte maturation after cotreatment with GnRH antagonist in high-risk OHSS patients [4]. Emergency medicine management rests upon disease recognition and subsequent appropriate resuscitation while avoiding unneces- sary or harmful interventions such as laparotomy or surgical intervention. In addition, the ED physician must be aware of the various complications seen both acutely and subacutely in these patients, to include thromboembolism, sepsis, pleural effusions, and adult respiratory distress syndrome.

Ovarian hyperstimulation syndrome is a critical diagnosis in emergency medicine and emergency physicians must

consider it in the differential for any female nontrauma patient presenting with hypotension, tachycardia, and abdominal pain.

Acknowledgment

All authors have contributed significantly to this study and the manuscript. All authors have approved this sub- mitted version. These opinions are those of the authors and do not necessarily represent those of the United States Army or the Department of Defense. The authors would like to thank Dr. Andrew Gjelsteen for his assistance with ultrasound images.

Michael A. Miller MD Department of Emergency Medicine Tripler Army Medical Center Honolulu, HI 95859, USA

Central Texas Poison Center Temple, TX 76508, USA

E-mail address: [email protected]

Eric Wirtz MD John Pease MD

Department of Emergency Medicine Tripler Army Medical Center Honolulu, HI 95859, USA

doi:10.1016/j.ajem.2007.11.032

References

  1. Binder H, Dittrich R, Einhaus F, Krieg J, Muller A, Strauss R, et al. Update on ovarian hyperstimulation syndrome: part 1–incidence and pathogenesis. Int J Fertil Womens Med 2007;52(1):11-26.
  2. Elchalal U, Schenker JG. The pathophysiology of ovarian hypersti- mulation syndrome–views and ideas. Hum Reprod 1997;12 (6):1129-37.
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  4. Engmann L, Diluigi A, Schmidt D, Nulsen J, Maier D, Benadiva C. The use of gonadotropin-releasing hormone (GnRH) agonist to induce oocyte maturation after cotreatment with GnRH antagonist in high-risk patients undergoing In vitro fertilization prevents the risk of ovarian hyperstimulation syndrome: a prospective randomized controlled study. Fertil Steril 2007 [electronic publication ahead of print].