Ovarian hyperstimulation syndrome (OHSS) is a serious complication of ovulation induction which, at present, is being studied increasingly because of its frequent occurrence as a result of the growing number of in-vitro fertilization (IVF) programmes. The anatomical changes involving enlargement of the ovaries and increased capillary permeability leading to acute fluid shift have been traditionally proposed to explain the different clinical features observed in OHSS. Recent work from our group, however, has shown that the pathogenesis of severe OHSS is more complex than currently understood and that marked peripheral arteriolar vasodilation is a major event in the development of the syndrome. Peripheral vasodilation may, in its turn, alter microvascular haemodynamics and permeability. This leads to a circulatory dysfunction with marked homeostatic activation of endogenous vasoactive systems having vasoconstrictor and sodium- and water-retaining activities. In this way, sodium and water retention would be a cause rather than a consequence of ascites formation in severe OHSS. This report analyses current concepts on body fluid regulations as well as neurohormonal and haemodynamic studies both in patients with severe OHSS and asymptomatic IVF women, integrating their findings into the present knowledge of the pathogenesis of the syndrome. Therapeutic implications are discussed.
Copyright (C) 1998, European Society of Human Reproduction and Embryology
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