A 28-Year-Old Writer With Bilious Vomiting After Egg Donation

Richard Lucidi, MD; Jordan Hylton, DO


May 28, 2021

Treatment for ovarian hyperstimulation syndrome is symptomatic. Spontaneous regression of disease typically occurs within 10-14 days. Close observation with serial abdominal examinations and weight checks may indicate improvement or deterioration in the clinical condition and may signify the onset of a further possible complication: torsion of the enlarged ovary. Sequential laboratory analysis also helps to distinguish any electrolyte abnormalities, which should be corrected.

Fluid maintenance is key in the treatment of ovarian hyperstimulation syndrome and must be carefully monitored. Fluid hydration usually begins with isotonic solutions to restore normal perfusion. Human albumin can also be considered. Diuretics are not recommended because they may contribute to intravascular volume depletion.

Prophylactic anticoagulation should be considered, given the risk for thromboembolism.[1,5] Paracentesis or pleurocentesis is performed if symptomatic ascites or pleural effusions develop. Surgical intervention is reserved for ovarian torsion or acute abdomen and is not routinely used for therapy.[5,7]

Prevention is key in limiting the life-threatening condition of ovarian hyperstimulation syndrome. Prevention typically occurs by withholding human chorionic gonadotropin injection if the ovaries are hyperstimulated, as determined by monitoring with estradiol levels and TVUS. Use of a gonadotropin-releasing hormone agonist or luteal support with progesterone instead of human chorionic gonadotropin may also help to reduce the occurrence of ovarian hyperstimulation syndrome. Albumin infusion and dopamine agonist administration, along with cabergoline administration at the time of oocyte retrieval, are also controversial alternatives that are used to prevent ovarian hyperstimulation syndrome. Aspiration of follicles within 36 hours of human chorionic gonadotropin injection may help to reduce the risk.[1,5,6]

The patient in this case was treated with antiemetics, pain medication, and intravenous hydration with normal saline. Her intake, output, and weight were carefully monitored, and she was anticoagulated with enoxaparin sodium throughout her hospital admission. Clostridium difficile, Shiga toxin, stool, blood, and urine cultures were performed on admission, and the findings were negative.

Owing to her fever, the patient was initially started on prophylactic antibiotics, which were discontinued after resolution of the fever within 48 hours. Her abdominal discomfort, nausea, and vomiting gradually improved so that she was ready for discharge on hospital day 4. She presented for follow-up 1 week later, and her symptoms had completely resolved. She had lost weight and had increased urinary frequency consistent with diuresis.


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