AN UNCOMMON CAUSE OF SEROSITIS Introduction Medically assisted procreation (MAP), includind in vitro fertilization (IVF) has evolved rapidly over the past two decades. Aiming to get better results, ovarian stimulation with exogenous hormones has been widely applied to increase the number of oocytes available for fertilization. Ovarian hyperstimulation syndrome (OHSS) is a rare (38% of IVF cycles are complicated by moderate or severe OHSS) and potentially fatal complication observed in some patients undergoing hormonal stimulation during MAP and has a varied spectrum of clinical and laboratory manifestations. The pathophysiology of OHSS is characterized by increased capillary permeability, leading to leakage of fluid from the vascular compartment, with third space fluid accumulation and intravascular dehydration. Women at higher risk of developing OHSS include those with polycystic ovaries, women under 30 years of age, use of GnRH agonists, development of multiple follicles during treatment, exposure to LH/hCG, and previous episodes of OHSS. Case report A 29 year-old nulligravid woman presented to the Emergency Room with complaints of: Dyspnea ; Lower abdominal pain ; Abdominal distension ; Nausea and vomit . These symptoms appeared 14 days following ovulation induction by Gonadotropin. Her physical examination revealed a distended, tender and tense abdomen with positive shifting dullness on percussion and vesicular murmur diminished at bases on pulmonary auscultation. Blood investigations showed hypoxemia, leukocytosis, hemoconcentration (hemoglobin of 16,7g/dl, hematocrit of 49%), low serum albumin, hyponatremia and a positive pregnancy test. The diagnosis of severe OHSS was confirmed by ultrasound scan revealing enlarged, multi-cystic ovaries, ascites and bilateral pleural effusion. Evolution and Treatment The treatment approach at the Emergency room consisted in: - Volume replacement (intravenous crystalloid fluids and albumin); - Monitoring vital signs and measuring central venous pressure; - Repeated ultrassound examination to assess the extent of ovarian enlargement and the degree of abdominal fluid accumulation; - Maintaining an adequate urine output and a negative hydric balance; - Prophylaxis for thromboembolic phenomena with LMWH. After initial stabilization, she was transferred to the Intensive Care Unit. Evolution of this case was favorable, and patient was later found to have a gemelar pregnancy. Suzane Ribeiro, Sérgio Janeiro, Susana Sousa, Susana Marques, Ermelinda Pedroso Serviço de Medicina Interna Centro Hospitalar de Setúbal, EPE - Hospital S. Bernardo References: 1. Mathur R, Evbuomwan I, Jenkins J. Prevention and management of ovarian hyperstimulation syndrome. Current Obstet Gynaecol 2005;15:1328. 2. Golan A, Ron-El R, Herman A, et al. Ovarian hyperstimulation syndrome: an update review. Obstet Gyncol Surv 1989;44:430-440; 3. The management of ovarian hyperstimulation syndrome. Royal College of Obstetricians and Gynaecologists Guideline No. 5 2006. 4. Aboulghar MA, Mansour RT. Ovarian hyperstimulation syndrome: classifications and critical analysis of preventive measures. Hum Reprod Update 2003;9(3):275-89. Laboratory and Imaging exams HEMATOLOGY Hb: 16,7 g/dL, Hct : 49% WBC: 30.900/µL, N- 90.8%, L- 6.7% Plat: : 378.000 U/L BLOOD CHEMISTRY Na: 129mEq/L Albumin: 1.3g/dL, Total protein: 3.30g/dL Arterial blood gas on room air showed hypoxemia (63mmHg) Urea: 39mg/dL, Creatinine: 0.9mg/dL CRP: 1.2mg/dL Positive Beta-HCG:107mUI/mL (<5.0) Normal thyroid hormones ABDOMINAL ULTRASOUND: Both ovaries were enlarged, polycystic, the right one measured 10,4x8,3X5,7cm and the left 11,4X8,2x6,3cm, each containing numerous enlarged follicles. Endometrial thickness and a significant amount of free fluid were observed in the abdomen and pelvis. The Liver and kidneys were normal. ECHOCARDIOGRAPHY: No sign of Pericardial effusion THORACIC X-RAY: Bilateral Pleural effusion Table 1. Classification of ovarian hyperstimulation syndrome (1) Figure 1: Chest X-ray revealed bilateral pleural effusion Conclusion OHSS can be classified as mild, moderate or severe. Severe cases, as the one we report, can be life-threatening and is characterized by growth of multiple large follicles with massive extravascular protein-rich fluid shift. This syndrom may range from electrolytic disorders, neurohormonal and haemodynamic changes, hypoalbuminemia, hemoconcentration to pulmonary manifestations, liver dysfunction, thromboembolic phenomena and febrile morbidity. Being familiar with this condition will lead to early recognition and will allow for an appropriate diagnostic and therapeutic management in order to prevent serious consequences. MILD MODERATE SEVERE CRITICAL Abdominal distension and discomfort, Ovarian size usually ‹8 cm. Moderate abdominal pain ; Nausea ± vomiting; Ultrasound evidence of ascites; Ovarian size usually 812 cm Clinical ascites (occasionally hydrothorax); Dyspneia; Oliguria; Haemoconcentration (haematocrit ›45%); Hypoproteinaemia; Ovarian size usually ›12 cm ; CrCL≥50 ml/min. Tense ascites or large hydrothorax; Haematocrit ›55%; WBC ›25 000/ml Oligo/anuria; Thromboembolic phenomena; Acute respiratory distress syndrome (ARDS) CrCL <50 ml/min. Figure 3: Abdominal and Pelvic ultrasound: Righ ovary Figure 2: Abdominal and Pelvic ultrasound: Endometrial thickness and Ascites.