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Table of Contents
CASE REPORT
Year : 2018  |  Volume : 1  |  Issue : 2  |  Page : 99-102

A case report on severe ovarian hyperstimulation syndrome in a pregnancy with torsion of bilateral enlarged ovaries with acute abdomen


Swagat Hospital and Research Centre, Bongaigaon, Assam, India

Date of Web Publication22-Feb-2019

Correspondence Address:
Sankar Kumar Das
Swagat Hospital and Research Centre, Dr. C.M Das Path, Bongaigaon, Assam
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/tofj.tofj_2_18

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  Abstract 


Ovarian hyperstimulation syndrome is a complication of fertility treatment, which uses pharmacological ovarian stimulation to increase the number of oocytes and therefore embryos available during assisted reproductive technology. Ovarian hyperstimulation syndrome is invariably associated with increased volume of ovaries which is itself a threat to undergo torsion, and it may cause an additional threat requiring prompt surgical intervention in many situations. Simple release of torsion, sacrificing the devitalized ovarian tissue in part and complete can have effect in continuation of pregnancy; and something like this happened in our case. The patient, 29-year-old, a known case of polycystic ovary syndrome (PCOS), conceived through ovulation induction; came with an episode of acute pain abdomen with abdominal distension toward the later part of her first trimester. Ultrasonography was done. Bilateral enlarged ovaries of around 23 cm × 11.8 cm each were seen meeting at the pouch of Douglas with ascites. It was a case of ovarian hyperstimulation syndrome, more specifically, a case of late ovarian hyperstimulation syndrome. Serum E2 level was 3263 pg/ml. Laparotomy was then done. Intraperitoneally bilateral ovarian torsion was seen with areas of necrosis. The right oophorectomy was done, while on the left side some portion of normal ovarian tissue was preserved. Following the operation, her symptoms were improved. The pregnancy continued uneventfully. Exposure of ovaries to human chorionic gonadotropin or luteinizing hormone following controlled ovarian stimulation by follicle-stimulating hormone underlies most cases of ovarian hyperstimulation syndrome. The risk of ovarian hyperstimulation syndrome is smaller when using gonadotropin-releasing hormone antagonist (GnRH) antagonist protocol instead of GnRH agonist protocol for suppression of ovulation during ovarian hyperstimulation. To avoid ovarian hyperstimulation syndrome, the best trigger is GnRH agonists. In PCOS patients, metformin is an important aid in reducing ovarian hyperstimulation syndrome.

Keywords: Acute abdomen, ovarian hyperstimulation syndrome, pregnancy, torsion


How to cite this article:
Das SK, Roy P. A case report on severe ovarian hyperstimulation syndrome in a pregnancy with torsion of bilateral enlarged ovaries with acute abdomen. Onco Fertil J 2018;1:99-102

How to cite this URL:
Das SK, Roy P. A case report on severe ovarian hyperstimulation syndrome in a pregnancy with torsion of bilateral enlarged ovaries with acute abdomen. Onco Fertil J [serial online] 2018 [cited 2019 Aug 24];1:99-102. Available from: http://www.tofjonline.org/text.asp?2018/1/2/99/252687




  Introduction Top


Ovarian hyperstimulation syndrome is a complication of fertility treatment, which uses pharmacological ovarian stimulation to increase the no of oocytes and therefore embryos available during assisted reproductive technology. It is associated with significant physical and psychological morbidity and has even been associated with maternal death. Ovarian hyperstimulation syndrome is invariably associated with increased volume of ovaries which is itself a threat to undergo torsion, and it may cause an additional threat requiring prompt surgical intervention in many situations. The simple release of torsion, sacrificing the devitalized ovarian tissue in part and complete can have effect in continuation of pregnancy; and something like this happened in our case. The key principles of ovarian hyperstimulation syndrome management are early recognition and the prompt treatment of the woman with moderate or severe ovarian hyperstimulation syndrome.[1]


  Case Report Top


The patient, a 29-year-old female was diagnosed to be a case of the bilateral polycystic ovarian syndrome in 2014, when she had approached the doctor for her irregular menses. She was on oral contraceptive pills for about a year, following which her cycles became regular, and she stopped the medication. Since then, she had a regular menstrual cycle of 28 ± 7 days with normal flow and duration of 7 days with no pain during menses. She is married for the past 5 years and is a second gravida with one spontaneous miscarriage at about 6 weeks of gestation, around 1 year back. She also had an IUI failure on 2015. Hysterosalpingography done on 2016 showed left tube fimbrial block. The present pregnancy was conceived through ovulation induction which was started on March 2018. Letrozole 2.5 mg twice a day was given from day 3 of menses to day 7. Human menopausal gonadotropin injection was given as 150 IU IM on alternate days from day3 of menses for a total of six doses. Her last menstrual period was on March 4, 2018. She was diagnosed as having early intrauterine pregnancy during the 2nd week of May 2018. Toward the later part of her first trimester, she had an episode of acute pain abdomen with abdominal distension. Ultrasonography was done. Bilateral enlarged ovaries of around 23 cm × 11.8 cm each were seen meeting at the pouch of douglas with ascites. It was a case of severe ovarian hyperstimulation syndrome, more specifically, a case of late ovarian hyperstimulation syndrome. Serum E2 level was 3263 pg/ml on June 5, 2018. Blood parameters as on June 6, 2018 were total leukocyte count 14,200 cells/cmm, serum sodium 132.8 mmol/l, serum potassium 5.5 mmol/l, hemoglobin 11 g/dl, and random blood sugar 94 mg/dl. Conservative treatment was given for 5 days after hospitalization. However, she had relapse on June 7, 2018. Laparotomy was then done. Intraperitoneally, bilateral ovarian torsion was seen with areas of necrosis. The right oophorectomy was done, while on the left side some portion of normal ovarian tissue was preserved. The sample was sent for biopsy. Biopsy showed hemorrhagic corpus luteal cyst with necrosis, hemorrhagic and infarction with no evidence of malignancy. Following the operation, her symptoms were improved. The pregnancy continued uneventfully. She was thereafter kept on iron-folic acid, calcium, multivitamin, and progesterone [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5].
Figure 1: Ultrasonography of the patient

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Figure 2: Pictures taken during operation

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Figure 3: Enlarged polycystic devitalized right ovary

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Figure 4: Enlarged polycystic left ovary

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Figure 5: Excised right ovary and portion of left ovary

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  Discussion Top


The exposure of ovaries to human chorionic gonadotropin (hCG) or luteinizing hormone following controlled ovarian stimulation by follicle-stimulating hormone (FSH) underlies most cases of Ovarian hyperstimulation syndrome. The exposure of hyperstimulated ovaries to hCG leads to the production of proinflammatory mediators, chief among which is vascular endothelial growth factor (VEGF), but a variety of cytokines are likely to be involved in the pathogenesis and clinical features of ovarian hyperstimulation syndrome.[2] Women with severe ovarian hyperstimulation syndrome demonstrate hypovolemia with a typical loss of 20% of their calculated blood volume in the acute phase of ovarian hyperstimulation syndrome.[3] Accompanying this hypovolemia is reduced serum osmolality and sodium. The parallel resetting of osmotic thresholds is thought to explain the observed decreases in serum osmolality and sodium as opposed to electrolyte losses.[4],[5] The diagnosis of ovarian hyperstimulation syndrome is made on clinical grounds. The typical patient presents with abdominal distension and discomfort following the trigger injection used to promote final follicular maturation before oocyte retrieval. The time of presentation following trigger injection divides patient into two groups.

  1. Early ovarian hyperstimulation syndrome = It usually presents within 7 days of hCG injection and usually associated with an excessive ovarian response
  2. Late ovarian hyperstimulation syndrome = Typically presents within ten or more days after hCG injection. The preceding ovarian response in such patients may be unremarkable. Late ovarian hyperstimulation syndrome tends to be more severe and prolonged than early ovarian hyperstimulation syndrome.[6]


Prevention of ovarian hyperstimulation syndrome

Risk of ovarian hyperstimulation syndrome is reduced by monitoring of FSH therapy to use this medication judiciously and by withholding the hCG medication. Cabergoline confers a significant reduction in the risk of ovarian hyperstimulation syndrome in high-risk woman according to Cochrane review of randomized trials, but the included trials did not report the live birth rates or multiple pregnancy rates.[7] Cabergoline as well other dopamine agonist might reduce the severity of ovarian hyperstimulation syndrome by interfering with the VEGF system.[8] The risk of ovarian hyperstimulation syndrome is smaller when using gonadotropin-releasing hormone antagonist (GnRH) antagonist protocol instead of GnRH agonist protocol for suppression of ovulation during ovarian hyperstimulation.[9] The underlying mechanism is that, with the GnRH antagonist protocol, initial follicular recruitment and selection is undertaken by endogenous endocrine factors before starting the exogenous stimulation, resulting in a smaller no of growing follicles when compared with the standard long GnRH agonist protocol.[9] The administration of albumin and hydroxyethyl starch confers a significant decrease in severe ovarian hyperstimulation syndrome, with no statistically significant evidence of decreased pregnancy rates.[7] Routine oocytes cryopreservation does not have evidence of preventing ovarian hyperstimulation syndrome.[7] Furthermore, coasting, which is ovarian hyperstimulation without induction of final maturation, does not significantly decrease risk of ovarian hyperstimulation syndrome[7] In case of the development of multiple follicles. Another option than completely cancelling the cycle is converting the cycle to rescue IVF. To avoid ovarian hyperstimulation syndrome, the best trigger is GnRH agonists.[10] This can also be considered when not performing a oocyte retrieval. Pregnancy rates after GnRH agonists trigger are lower due to luteal phase deficiency.[11] Freezing all embryos and replacing them in a subsequent cycle would be a valid strategy. In polycystic ovary syndrome patients, metformin is an important aid in reducing ovarian hyperstimulation syndrome.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Royal College of Obstetricians and Gynecologists. The Management of Ovarian Hyperstimulation Syndrome. Green-top Guideline no. 5.; Febraury, 2016.  Back to cited text no. 1
    
2.
Braat DD, Schutte JM, Bernardus RE, Mooij TM, van Leeuwen FE. Maternal death related to IVF in the Netherlands 1984-2008. Hum Reprod 2010;25:1782-6.  Back to cited text no. 2
    
3.
Evbuomwan IO, Davison JM, Murdoch AP. Coexistent hemoconcentration and hypoosmolality during superovulation and in severe ovarian hyperstimulation syndrome: A volume homeostasis paradox. Fertil Steril 2000;74:67-72.  Back to cited text no. 3
    
4.
Evbuomwan IO, Davison JM, Baylis PH, Murdoch AP. Altered osmotic thresholds for arginine vasopressin secretion and thirst during superovulation and in the ovarian hyperstimulation syndrome (OHSS): Relevance to the pathophysiology of OHSS. Fertil Steril 2001;75:933-41.  Back to cited text no. 4
    
5.
Evbuomwan I. The role of osmoregulation in the pathophysiology and management of severe ovarian hyperstimulation syndrome. Hum Fertil (Camb) 2013;16:162-7.  Back to cited text no. 5
    
6.
Mathur RS, Akande AV, Keay SD, Hunt LP, Jenkins JM. Distinction between early and late ovarian hyperstimulation syndrome. Fertil Steril 2000;73:901-7.  Back to cited text no. 6
    
7.
Farquhar C, Rishworth JR, Brown J, Nelen WL, Marjoribanks J. Assisted reproductive technology: An overview of cochrane reviews. Cochrane Database Syst Rev 2014;12:CD010537.  Back to cited text no. 7
    
8.
Gomez R, Gonzalez-Izquierdo M, Zimmermann RC, Novella-Maestre E, Alonso-Muriel I, Sanchez-Criado J, et al. Low-dose dopamine agonist administration blocks vascular endothelial growth factor (VEGF)-mediated vascular hyperpermeability without altering VEGF receptor 2-dependent luteal angiogenesis in a rat ovarian hyperstimulation model. Endocrinology 2006;147:5400-11.  Back to cited text no. 8
    
9.
La Marca A, Sunkara SK. Individualization of controlled ovarian stimulation in IVF using ovarian reserve markers: From theory to practice. Hum Reprod Update 2014;20:124-40.  Back to cited text no. 9
    
10.
Humaidan P, Kol S, Papanikolaou EG; Copenhagen GnRH Agonist Triggering Workshop Group. GnRH agonist for triggering of final oocyte maturation: Time for a change of practice? Hum Reprod Update 2011;17:510-24.  Back to cited text no. 10
    
11.
Engmann L, Benadiva C, Humaidan P. GnRH agonist trigger for the induction of oocyte maturation in GnRH antagonist IVF cycles: A SWOT analysis. Reprod Biomed Online 2016;32:274-85.  Back to cited text no. 11
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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