Severe ovarian hyperstimulation syndrome: Role of peripheral vasodilation

Abstract

Objective To investigate the pathogenesis of the systemic hemodynamic disturbance and the renal production of vasodilator prostaglandins (PGs) in the ovarian hyperstimulation syndrome. Design Prospective longitudinal study. Setting Assisted Reproduction Unit of the Hospital Clinic i Provincial in Barcelona. Patients Five in vitro fertilization patients with ascites because of severe ovarian hyperstimulation syndrome. Main Outcome Measures Measurement during the syndrome and 4 weeks after recovery of the following: cardiac output, arterial pressure, estimated peripheral vascular resistances, hematocrit, standard renal function tests, plasma renin activity, plasma aldosterone, norepinephrine and antidiuretic hormone concentrations, and urinary excretion of PGE 2 and 6-keto-PGF 1α . Results During the syndrome, all patients showed arterial hypotension (74.2±3.8 versus 85.8±1.0mm Hg), tachycardia, increased cardiac output (6.4±0.2 versus 4.4±0.1L/min), low peripheral vascular resistance (929±52 versus 1,568±51dyn/sec per cm −5 ), high plasma levels of renin (72±25 versus 0.5±0.1ng/mL per h −1 ), norepinephrine (639±141 versus 203±21pg/mL) and antidiuretic hormone (6.1±1.6 versus 1.5±0.1pg/mL), and increased urinary excretion of PGE 2 (551±152 versus 106±44pg/min) and 6-keto-PGF 1α (470±76 versus 99±11pg/min). No evidence of hemoconcentration, as assessed by hematocrit, was observed in any patient. Conclusions (1) Severe ovarian hyperstimulation syndrome is related to marked arteriolar vasodilation that leads to underfilling of the arterial vascular compartment and stimulation of endogenous vasoconstrictor systems and (2) the increased urinary excretion of PGs probably represents a homeostatic response to antagonize the renal effects of these systems.