The first patient was admitted to the hospital for management of severe ovarian hyperstimulation syndrome (OHSS). She required management with albumin for intravascular volume repletion and anticoagulation with heparin. Later in the hospitalization, she required a therapeutic paracentesis with 2.5 L of fluid drained and was discharged 5 days after admission to close follow-up with OBGYN.
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ACEP Now: April Digital 02-DThe second patient was admitted to the hospital with moderate OHSS. Ultimately, she only required supportive care and heparin for anticoagulation. She was discharged 2 days later.
OHSS is attributed to overstimulation of the ovaries from an assisted reproductive therapy (ART) cycle. Risk factors for OHSS include age younger than 30 years old, large number of follicles or eggs retrieved, history of polycystic ovary syndrome or OHSS, low BMI, and embryo transfer that results in pregnancy right after IVF.1 The incidence of severe OHSS is between 0.1% to 2.0%, however mild cases may be as common as 20% to 33%.1,2
In an ART cycle, and during the ovarian stimulation stage, gonadotropins are administered to stimulate multiple follicles to develop simultaneously. Final oocyte maturation is sometimes assisted with the administration of human gonadotropin hormone (hCG) 1-3 days before retrieval.
OHSS is caused by increased capillary permeability, mainly from vascular endothelial growth factor (VEGF) secreted from granulosa cells causing a shift of fluid from intravascular spaces to extravascular spaces. hCG (given in IVF) triggers this increased secretion of VEGF. hCG can also activate the renin-angiotensin-aldosterone pathway in the ovaries to exacerbate the fluid accumulation.3 This leads to intravascular hypovolemia with extravascular fluid accumulations such as ascites and pleural effusions. Peritonitis may result from the release of inflammatory compounds or irritation from hemoperitoneum caused by cyst rupture.
Mild OHSS generally causes mild abdominal pain and distension, while severe OHSS is caused by large ovarian cysts leading to hyponatremia, hypoproteinemia, hyperkalemia, hydrothorax, renal injury, and hypovolemic shock.4 (Table 1)
Diagnosis includes clinical features such as abdominal pain, bloating, and decreased urine output after ovarian stimulation followed by hCG administration. Examination will often show shifting dullness on abdominal examination due to ascites, with intraperitoneal fluid and significantly enlarged ovaries visualized on transvaginal ultrasound.5
OHSS is generally treated with symptomatic management. Treatment with albumin and fluids can increase intravascular oncotic pressure to increase intravascular fluid volume.4 Paracentesis and thoracentesis may be performed for relief of severe pain and shortness of breath, as well as if a patient becomes hemodynamically unstable or oliguric.6 Patients do require anticoagulation with low molecular weight heparin. Although there is currently no single cause of hyper-coagulability in OHSS, studies have shown there is an increased risk of thrombosis likely from hemoconcentration and alterations in the hemostatic pathways.7
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