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Rizk et al. (1997) have extensively reviewed the pathophysiology of OHSS.
OHSS is marked by massive bilateral cystic ovarian enlargement (Figure I.1).
The ovaries are noted to have a signi¬cant degree of stromal edema,
interspersed with multiple hemorrhagic follicular and theca-lutein cysts, areas
of cortical necrosis and neovascularization. The second pathological phenom-
enon is that of acute body ¬‚uid shifts, resulting in ascites (Figure I.2) and
pleural effusion. Most investigators believe that these ¬‚uid shifts are the result
of enhanced capillary permeability (Rizk and Aboulghar, 1991, 1999; El-Chalal
and Schenker, 1997; Kaiser, 2003). This has been demonstrated in several
animal models including hyperstimulated rats (Gomez et al., 2002), and rabbits
(Schenker and Weinstein, 1978). More recently, Tollan et al. (1990) showed
that, during ovarian stimulation for IVF, there is in¬ltration of ¬‚uid from the
vascular space to the interstitial compartment one day before oocyte aspiration.
Signi¬cant advances have been made in our understanding of the nature of the
vasoactive agents involved (Figure III.1).


In contrast to our classic concept of increased capillary permeability (Rizk,
1993a, b; Aboulghar et al., 1996; Rizk et al., 1997). Balasch et al. (1991) adopted
a very different and interesting view. They studied the hemodynamic changes in
severe OHSS and suggested that the circulatory disturbances are not secondary
to reduction in circulating blood volume, but are a consequence of an intense
peripheral arteriolar vasodilatation that leads to under¬lling of the arterial
vascular component, arterial hypotension and a compensatory increase in heart
rate and cardiac output (Balasch et al., 1991). During the syndrome, all ¬ve
patients studied showed arterial hypotension, tachycardia, increased cardiac
output and low peripheral vascular resistance. They observed high plasma levels
of renin, norepinephrine and antidiuretic hormone and increased urinary
excretion of PGE2 and 6-keto-PGF1a. However, it must be mentioned that none
of their patients in this study had hemo-concentration À a common ¬nding
among patients with severe OHSS. Balasch et al. (1994) evaluated endogenous
vasoactive neurohormonal factors and renal function in 31 patients with severe
OHSS. These patients were evaluated at the appearance of the syndrome and
four to ¬ve weeks later after the condition resolved. They recorded increased
hematocrit and cardiac output, and decreased mean arterial pressure and


Fig. III.1: Pathophysiology of OHSS. TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor;
RAS, reninÀangiotensin system

peripheral vascular resistance. This was accompanied by marked increases in
plasma renin, norepinephrine, antidiuretic hormone, and atrial natriuetic
peptide. Hemoconcentration was observed in 50% of the patients. Balasch et al.
(1994) analyzed these results with and without hemoconcentration. They
observed similar values for cardiac output, arterial pressure and peripheral
vascular resistance. However, higher levels of renin, norepinephrine and

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