Tension Hydrothorax as a Rare Presentation of Ovarian Hyperstimulation Syndrome

Abstract

INTRODUCTION: Pleural effusions in ovarian hyperstimulation syndrome (OHSS), whether transudative or exudative, can occur in up to 30% of cases. However, it is exceedingly uncommon for them to present as a tension hydrothorax requiring emergent intervention. We report on just such a case. CASE PRESENTATION: A 29-year-old female presented to our emergency department (ED) for chest pain and dyspnea. She had no previous medical history. She was being followed by reproductive medicine for in vitro fertilization which was preceded by ovarian hyperstimulation with human chorionic gonadotropin (hCG) 17 days previously. She had two embryos successfully implanted 7 days before presentation. She had complained of some increased dyspnea several days prior to her ED visit as well as some intermittent nausea. In the ED she was in moderate respiratory distress with complaints of abdominal pain and nausea. She was found to be afebrile with respirations of 20-25 breaths per minute, heart rate 130 beats per minute, and blood pressure of 116/80 mm Hg. She had decreased breath sounds over the right hemi-thorax. Her oxygenation was 98% on 2L oxygen per minute. There were no other remarkable physical findings. Laboratory investigations revealed a white blood count 23.2 thousand per cubic millimeter, hematocrit 48.8%, albumin 3.0 g/dL, and hCG 220 mIU/mL. Computed tomography of the chest revealed a right tension hydrothorax and no pulmonary embolus. Trans-vaginal ultrasound revealed bilaterally enlarged ovaries. During her hospital stay she required six therapeutic thoracenteses for a total volume of 9.6L removed. Her pleural fluid analysis revealed an exudative effusion by Light's criteria. DISCUSSIONS: Defined as a loss of control over hyperstimulation, OHSS complicates up to 33% of hyperstimulation cases which ranges both in severity and presentation. Vascular endothelial derived growth factor is thought to mediate much of the fluid shifts in these cases through increased capillary permeability. There are several thoughts as to why pleural effusions may develop in these cases and why they develop more on the right than left. They may result from both the positive intra-abdominal pressures and presence of diaphragmatic defects. The ascitic fluid is then allowed to move along a pressure gradient from the abdomen into the pleural space. Also, right sided pleural effusions may occur more often due to decreased lymphatic drainage when compared to the left side. Interestingly, our patient had a relatively small amount of ascites; however, this may have in fact been due to the continuous movement of fluid into the pleural space. Only 4.5% of reported severe cases have required therapeutic thoracenteses. In its severe form patients with OHSS may show objective evidence of hemoconcentration, acute kidney injury, electrolyte abnormalities, and liver dysfunction. They can also show clinical signs of hypotension, abdominal pain, vomiting, and diarrhea. OHSS is a pro-thrombotic state and thromboembolism is the most feared complication. Fortunately, our patient did not suffer a pulmonary embolus, but she did have a tension hydrothorax requiring immediate thoracentesis Based on the reported literature our patient required the second largest therapeutic volume removed. CONCLUSION: Severe OHSS cases presenting with massive hydrothoraces may benefit from early placement of a small chest tube with daily volume removal until fluid re-accumulation subsides.